text:
\section{Introduction}
Let $A$ denote the class of the functions $f$ of the form
\begin{equation}\label{eg:}
    f(z)=z+\sum^{\infty}_{n=2} a_{n}z^{n}
\end{equation}
which are analytic in the open unit disc $ U=\{z\in C:|z|<1$\} and satisfy the normalization
condition $f(0)=f^{'}(0)-1=0$. Let $S$ be the subclass of A consisting of functions of the form (1) which are also univalent in $U$.

 A function $f\in A$  is said to be in the class of strongly bi-starlike functions of order $\alpha (0<\alpha\leq1)$,
denoted by $S^{*}_{\Sigma}(\alpha)$, if each of the following conditions is satisfied:

\begin{center}
$\left|\arg\left\{\frac{zf^{'}(z)}{f(z)}\right\}\right|<\frac{\alpha\pi}{2}, (|z|<1, 0<\alpha\leq1),$
\end{center}
and
\begin{center}
$\left|\arg\left\{\frac{zg^{'}(w)}{g(w)}\right\}\right|<\frac{\alpha\pi}{2}, (|w|<1, 0<\alpha\leq1),$
\end{center}
where $g$ is the extension of $f^{-1}$ to $U$ (for details see ( Brannan and Taha \cite{Brannan}).
And is said to be in the class of strongly bi-convex functions of order $\alpha(0<\alpha\leq1)$, denoted by $K_{\Sigma}(\alpha)$, if it
satisfies the following inequality
\begin{center}
$\left|\arg\left\{{1+\frac{zf^{''}(z)}{f^{'}(z)}}\right\}\right|<\frac{\alpha\pi}{2}, (|z|<1, 0<\alpha\leq1)$.
\end{center}
and

\begin{center}
$\left|\arg\left\{{1+\frac{wg^{''}(w)}{g^{'}(w)}}\right\}\right|<\frac{\alpha\pi}{2}, (|w|<1, 0<\alpha\leq1)$.
\end{center}
Where $g$ is the extension of $f^{-1}$ to $U$ .
Recall that the Koebe one-quarter theorem \cite{Duren2} ensures that the image of $D$ under every
univalent function $f\in S$ contains a disk of radius $\frac{1}{4}$. Thus every univalent function $f$
has an inverse $f^{-1}$ satisfying $f^{-1}(f(z)) = z$, $(z\in D)$ and
\begin{center}
$f^{-1}(f(w)) = w$, $(|w|<r_{0}f, r_{0}f\geq\frac{1}{4})$.
\end{center}
\begin{equation}\label{eg:}
         g(w)=w-a_{2}w^{2}+(2a_{2}^{2}-a_{3})w^{3}-(5a_{2}^{2}-5a_{2}a_{3}+a_{4})w^{4}+...\ .
\end{equation}
In recent years, many authors  discussed estimate on the
coefficients $|a_{2}|$ and  $|a_{3}|$ for subclasses of bi-univalent function (see for example \cite{Srivastava}, \cite{Frasin}, \cite{Alamoush1}, \cite{Alamoush2}, \cite{Alamoush3}, \cite{Alamoush4}).

Let $f:D\rightarrow C$ be an analytic function on $D$ having taylor expansion $f(z)=\Sigma^{\infty}_{n=1} a_{n}z^{n}, z\in D,$ with $a_{n}\in C$,\ $a_{1}=1 $ $,n=1,2,3,...\ .$ A function $f\in S$ is bi-univalent in $D$ if both $f$ and $f^{-1}$ are univalent in $D$.

\begin{flushleft}
The object of the present paper is to introduce a new subclasses of the function
class $\Sigma$ and to find estimates on the coefficients $|a_{2}|$ and  $|a_{3}|$ for new functions in these new subclasses of the function
class $\Sigma$.
 \begin{flushleft}

 We say that $\delta_{n}^{\alpha}f(z)$ is  The $n^{th}$ Cesaro mean of order $\alpha\geq0$ of $f$ is defined by
 \end{flushleft}

\ \\
\end{flushleft}
\begin{center}
$\delta_{n}^{\alpha}f(z)=z+\sum^{\infty}_{n=2}A_{n} a_{n}z^{n}$
\end{center}
where
 \begin{center}
$ A_{n}=   {\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-n\\ k-n \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-1 \\ k-n\end{array}} \right ) } \end{array}},\ a_{1}=1.   $
\\

\end{center}
Let $D$ denote the open unit disk in $C$. It is well known that outer functions are zero-free on the unit disk. Outer functions, which play an important role in $H_{p}$ theory to find a suitable finite (polynomial) approximation for the outer infinite series $f$ so that the approximant reduces the zero-free property of $f$, arise in the characteristic equation which determines the stability of certain nonlinear systems of differential equations. Recall that an outer function is a function $f \in H_{p}$ of the form
\begin{center}

$f(z) = e^{i \gamma} e^{ \frac{1} {2 \pi} \int _{-\pi} ^ {\pi}
\frac{1 + e^{it}z} {1-e^{it}z} \log \psi (t)dt }$
\end{center}

\noindent where  $\psi(t) \geq 0$,    $\log  \psi(t)$   is in $L^1$ and  $\psi(t)$ is in $L^p$.  See \cite{Duren1} for the definitions and classical properties of outer functions.  Since any function $f$ in $H^1$ which has $1/f$ in $H^1$ is an outer function, then typical examples of outer functions can be generated by functions of the form
$\prod _ {k=1} ^ n (1 - e^{i \theta _ k}z)^{\alpha _ k}$ for $-1 <  \alpha _k < 1$.

We observe for outer functions that the standard Taylor approximants do not, in general, retain
the zero-free property of $f$. It was shown in \cite{Barnard} that the Taylor approximating polynomials to outer functions can vanish in the unit disk. By using convolution methods that the classical Cesaro means, retains the zero-free property of the derivatives of bounded convex functions in the unit disk. The classical Cesaro means play an important role in geometric function theory (see \cite{Ruscheweyh1},\cite{Ruscheweyh2}).

\begin{lem}

\textit{If $h\in p$  then $|c_{k}|<1,$  for each $k$, where $p$ is the family of all functions $h$ analytic in $U$ for which $\Re\{h(z)\}>0$, then}
\begin{center}
$h(z)=1+c_{1}z+c_{2}z^{2}+c_{3}z^{3}+...\ , z\in U$.
\end{center}
\end{lem}
\section{COEFFICIENT BOUNDS FOR THE FUNCTION CLASS $H_{\Sigma}(\psi)$}

In the sequel, it is assumed that $\varphi$ . is an analytic function with positive real part in the
unit disk $D$, satisfying $\psi(0) = 1, \psi^{'}(0) > 0$, and $\psi(D)$ is symmetric with respect to the real
axis. Such a function has a Taylor series of the form
\begin{center}
\begin{equation}\label{eg:}
    \psi(z)=1+B_{1}z+B_{2}z^{2}+B_{3}z^{3}+...., (B_{1}>0).
\end{equation}
\end{center}
Suppose that $u(z)$ and $v(z)$ are analytic in the unit disk D with $u(0) = v(0) = 0$,
$|u(z)| < 1,|v(z)| < 1$, and suppose that

\begin{center}
\begin{equation}\label{eg:}
u(z)=b_{1}z+\sum^{\infty}_{n=2} b_{n}z^{n}, v(z)=c_{1}z+\sum^{\infty}_{n=2} c_{n}z^{n},(|z|<1).
\end{equation}
\end{center}

It is well known that

\begin{center}
\begin{equation}\label{eg:}
|b_{1}|\leq1, |b_{2}|\leq1-|b_{1}|^{2},  |c_{1}|\leq1 , |c_{2}|\leq1-|c_{1}|^{2}.
\end{equation}
\end{center}

By a simple calculation, we have

\begin{center}
\begin{equation}\label{eg:}
\psi(u(z))=1+B_{1}b_{1}z+(B_{1}b_{2}+B_{2}b^{2}_{1})z^{2}+...\ , |z|<1
\end{equation}
\end{center}
and

\begin{center}
\begin{equation}\label{eg:}
\psi(v(w))=1+B_{1}c_{1}w+(B_{1}c_{2}+B_{2}c^{2}_{1})w^{2}+...\ , |w|<1.
\end{equation}
\end{center}

\begin{Definition}
\cite{Ali} A function $f\in \Sigma$ is said to be in the class $H_{\Sigma}(\psi)$ if and only if
\begin{center}
$f^{'}(z) \prec \psi(z),g^{'}(z) \prec \psi(w)$,
\end{center}
where $g(w) = f^{-1}(w)$.
\end{Definition}

\begin{thm}
\label{eg:}
If $f$ given by (1) is in the class $H_{\Sigma}(k,\psi)$, then

\begin{center}
\begin{equation}\label{eg:}
|a_{2}|\leq\left|\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-2 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-2 \\ k-2\end{array}} \right ) } \end{array}\right|\frac{B_{1}\sqrt{B_{1}}}{\sqrt{[|3B^{2}_{1}-4B_{2}|+4B_{1}]}}
\end{equation}
\end{center}

\begin{flushleft}
and
\end{flushleft}

\begin{equation}\label{eg:}
    |a_{3}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-3 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-3 \\ k-3\end{array}} \right ) } \end{array}\right]\left[(1-\frac{4}{3B_{1}})\frac{B^{3}_{1}}{{[|3B^{2}_{1}-4B_{2}|+4B_{1}]}}+\frac{B_{1}}{3}\right].
\end{equation}
\end{thm}

\begin{proof}
Let $f\in H_{\Sigma}(k,\psi)$  and $g = f^{-1}$. Where $a_{1}=1$ . Then there are analytic functions $u, v : D \rightarrow D$
given by (4) such that
\begin{equation}\label{eg:}
    [\delta_{n}^{\alpha}f(z)]^{'}=\psi(u(z)),  [\delta_{n}^{\alpha}g(w)]^{'}=\psi(v(w)),
\end{equation}

since

\begin{center}
\begin{equation}\label{eg:}
    [\delta_{n}^{\alpha}f(z)]^{'}=1+2 A_{2}a_{2}z+3 A_{3}a_{3}z^{3}+...\ ,
\end{equation}
\end{center}
\begin{center}
$[\delta_{n}^{\alpha}g(w)]^{'}=1-2A_{2}a_{2}w+3[2 A_{2}^{2}a^{2}_{2}-A_{3}a_{3}]w^{3}+...\ ,$
\end{center}
it follows from (6), (7), (10) and (11) that
\begin{center}
\begin{equation}\label{eg:}
    2A_{2}a_{2}=B_{1}b_{1},
\end{equation}
\begin{equation}\label{eg:}
    3A_{3}a_{3}=B_{1}b_{2}+B_{2}b^{2}_{1},
\end{equation}
\end{center}

\begin{center}
\begin{equation}\label{eg:}
   - 2A_{2}a_{2}=B_{1}c_{1},
\end{equation}
\end{center}

\begin{center}
\begin{equation}\label{eg:}
3[2A^{2}_{2}a^{2}_{2}-A_{3}a_{3}]=B_{1}c_{2}+B_{2}c^{2}_{1}.
\end{equation}
\end{center}
From (12) and (14), we get
\begin{center}
\begin{equation}\label{eg:}
b_{1}=-c_{1}.
\end{equation}
\end{center}
By adding (15) to (13), further computations using (12) and (16) lead to

\begin{center}
\begin{equation}\label{eg:}
A_{2}^{2}a_{2}^{2}[3B^{2}_{1}-8B_{2}]=B_{1}^{3}(b_{2}+c_{2}).
\end{equation}
\end{center}
Also, from (16) and  (17), together with (5), we obtain

\begin{center}
\begin{equation}\label{eg:}
|A_{2}^{2}a_{2}^{2}[3B^{2}_{1}-8B_{2}]|\leq2 B_{1}^{3}(1-|b_{1}|^{2}).
\end{equation}
\end{center}
From (12) and (18) we get
\begin{center}
$|a_{2}|\leq\left|\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-2 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-2 \\ k-2\end{array}} \right ) } \end{array}\right|\frac{B_{1}\sqrt{B_{1}}}{\sqrt{[|3B^{2}_{1}-4B_{2}|+4B_{1}]}}$.
\end{center}

Which, in view of the well-known inequalities $|b_{2}|\leq 2$ and $|c_{2}|\leq 2$ for functions with positive real part, gives us the desired estimate on $|a_{2}|$ as asserted in (8).
By subtracting (15) from (13), further computations using (12) and (16) lead to
\begin{center}
\begin{equation}\label{eg:}
6A_{3}a_{3}=6A_{2}^{2}a^{2}_{2}+B_{1}(b_{2}-c_{2}).
\end{equation}
\end{center}
From (5), (12), (16) and (19), it follows that

\begin{center}
$|a_{3}|=\frac{6A_{2}^{2}|a_{2}|^{2}+B_{1}(|b_{2}|+|c_{2}|)}{6A_{3}}$
\end{center}
\begin{center}
$\leq\frac{6A_{2}^{2}|a_{2}|^{2}+B_{1}(1-|b_{1}|^{2})+(1-|c_{1}|^{2})}{6A_{3}}$
\end{center}

\begin{center}
$\leq\frac{[1-\frac{4}{3B_{1}}]A_{2}^{2}|a_{2}|^{2}}{A_{3}}+\frac{B_{1}}{3A_{3}}$
\end{center}

\begin{center}
$|a_{3}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-3 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-3 \\ k-3\end{array}} \right ) } \end{array}\right]\left[(1-\frac{4}{3B_{1}})\frac{B^{3}_{1}}{{[|3B^{2}_{1}-4B_{2}|+4B_{1}]}}+\frac{B_{1}}{3}\right]$.
\end{center}
\end{proof}

\section{COEFFICIENT BOUNDS FOR THE FUNCTION CLASS $Q_{\Sigma}(\alpha,\mu,\lambda)$ }

\begin{Definition}
\textit{A function $f(z)$ given by (1) is said to be in the class $Q_{\Sigma}(\alpha,\mu,\lambda)$   if the following conditions are satisfied}: For $f\in \Sigma,$
\\
\begin{equation}\label{dlabel}
 \left|arg\left\{\frac{(1-\lambda)\delta^{\alpha}_{_{n}}f(z)+\lambda z[\delta^{\alpha}_{_{n}}f(z)]'}z\right\}\right|<\frac{\pi\alpha}{2}, \alpha(0 <\alpha \leq 1, \lambda\geq1, z\in U),
\end{equation}
\begin{flushleft}
and
\end{flushleft}
\begin{equation}\label{eg:}
\left|arg\left\{\frac{(1-\lambda)\delta^{\alpha}_{_{n}}g(w)+\lambda w[\delta^{\alpha}_{_{n}}g(w)]'}w\right\}\right|<\frac{\pi\alpha}{2},\alpha(0 <\alpha \leq 1,\lambda\geq1, w\in U),
\end{equation}
\begin{flushleft}
where the function $g$ defined by (2).
\end{flushleft}
\end{Definition}

   \begin{thm}
\textit{
Let the function $f(z)$ given by (1) be in the class $Q_{\Sigma}(\alpha,\mu,\lambda)$,
$n\in N_{0},0\leq\beta<1, \lambda\geq1$. Then}
\begin{equation}\label{eg:}
|a_{2}|\leq2\alpha\left|\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-2 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-2 \\ k-2\end{array}} \right ) } \end{array}\right|\frac{{1}}{\sqrt{4^{k}(1+\lambda)^{2}+\alpha[2.3^{k}(1+\lambda)-4^{k}(1+\lambda)^{2}]}},
\end{equation}
and
\begin{equation}\label{eg:}
|a_{3}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-3 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-3 \\ k-3\end{array}} \right ) } \end{array}\right]\left[\frac{2\alpha}{(1+2\lambda)}+\frac{4\alpha^{2}}{(1+\lambda)^{2}}\right].\end{equation}

\end{thm}
\begin{proof}
From (20) and (21), we can write
\begin{equation}\label{eq:}
\frac{(1-\lambda)\delta^{\alpha}_{_{n}}f(z)+\lambda z[\delta^{\alpha}_{_{n}}f(z)]'}z=[p(z)]^{\alpha},
\end{equation}
and

\begin{equation}\label{eq:}
\frac{(1-\lambda)\delta^{\alpha}_{_{n}}g(w)+\lambda w[\delta^{\alpha}_{_{n}}g(w)]'}w=[q(w)]^{\alpha},
\end{equation}
where $p(z)$ and $q(w)$ in $P$ and  $a_{1}=1$, and have the forms

\begin{equation}\label{eq:}
p(z)=1+p_{1}z+p_{2}z^{2}+p_{3}z^{3}+...\ \ ,
\end{equation}
and
\begin{equation}\label{eq:}
q(w)=1+p_{1}w+q_{2}w^{2}+q_{3}w^{3}+...\ \ .
\end{equation}
Now, equating the coefficients in (24) and (25), we obtain
\begin{equation}\label{eg:}
    (1+\lambda)A_{2}a_{2}=\alpha p_{1},
\end{equation}
\begin{equation}\label{eg:}
        (1+2\lambda)A_{3}a_{3}=\frac{1}{2}[2\alpha p_{2}+\alpha(\alpha-1)p_{1}^{2}],
\end{equation}
\begin{equation}\label{eg:}
    - (1+\lambda)A_{2}a_{2}=\alpha q_{1},
\end{equation}
\begin{equation}\label{eg:}
   (1+2\lambda)[2A_{2}^{2}a^{2}_{2}-A_{3}a_{3}]=\frac{1}{2}[2\alpha q_{2}+\alpha(\alpha-1)q_{1}^{2}].
\end{equation}
From (28) and (30), we obtain
\begin{equation}\label{eg:}
p_{1}=-q_{1}
\end{equation}
and
\begin{equation}\label{eg:}
         2(1+\lambda)^{2}A_{2}^{2}a^{2}_{2}=\alpha ^{2}(p^{2}_{1}+q^{2}_{1}).
\end{equation}
Now, from (29), (31) and (33), we obtain

\begin{center}
       $  2(1+2\lambda)A_{2}^{2}a^{2}_{2}=\alpha (p_{2}+q_{2})+\frac{1}{2}[2\alpha(\alpha-1)(p_{1}^{2}+q_{1}^{2})]$
\end{center}

\begin{center}
$=\alpha(p_{2}+q_{2})+\frac{\alpha(\alpha-1)}{2}.\frac{2(1+\lambda)^{2}A_{2}^{2}a^{2}_{2}}{\alpha^{2}}\ .$
\end{center}
Therefore we have

    \begin{center}
    $a^{2}_{2}=\frac{\alpha^{2}(p_{2}+q_{2})}{[(1+\lambda)^{2}+\alpha[(1+2\lambda)]-\lambda^{2}]]A_{2}^{2}}\ .$
    \end{center}

 Applying Lemma 1.1 for the coefficients $p_{2}$ and $q_{2}$, we immediately have
\begin{center}
 $|a_{2}|\leq2\alpha\left|\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-2 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-2 \\ k-2\end{array}} \right ) } \end{array}\right|\frac{{1}}{\sqrt{4^{k}(1+\lambda)^{2}+\alpha[2.3^{k}(1+\lambda)-4^{k}(1+\lambda)^{2}]}}$.
\end{center}
This gives the bound as asserted in (22).

Next, in order to find the bound on $|a_{3}|$, we subtract (29) from (31) and obtain
\begin{center}
\begin{quote}
\begin{center}
$2[(1+2\lambda)(A_{3}a_{3}-A_{2}^{2}a^{2}_{2})$
\end{center}
\end{quote}
=$\frac{1}{2}(2\alpha(p_{2}-q_{2})+\alpha(\alpha-1)(p^{2}_{1}-q^{2}_{1})),$
\end{center}

\begin{center}
$a_{3}=\frac{\alpha(p_{2}-q_{2})}{2(1+2\lambda)A_{3}}+\frac{\alpha^{2}(p^{2}_{1}+q^{2}_{1})}{2(1+\lambda)^{2}A_{3}}$,
\end{center}

\begin{center}
$a_{3}=\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-3 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-3 \\ k-3\end{array}} \right ) } \end{array}\right]\left[\frac{\alpha(p_{2}-q_{2})}{2(1+2\lambda)}+\frac{\alpha^{2}(p^{2}_{1}+q^{2}_{1})}{2(1+\lambda)^{2}}\right]$,
\end{center}
 Applying Lemma 1.1 for the coefficients $p_{2}$ and $q_{2}$, we immediately have
\begin{center}
$|a_{3}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-3 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-3 \\ k-3\end{array}} \right ) } \end{array}\right]\left[\frac{2\alpha}{(1+2\lambda)}+\frac{4\alpha^{2}}{(1+\lambda)^{2}}\right]$.
\end{center}

This completes the proof of Theorem 3.2.
\end{proof}

\section{COEFFICIENT BOUNDS FOR THE FUNCTION CLASS   $H_{\Sigma}(\beta,\mu,\lambda)$ }

\begin{Definition}
\textit{
A function $f(z)$ given by (1) is said to be in the class $H_{\Sigma}(\beta,\mu,\lambda)$  if the following conditions are satisfied: For $f\in \Sigma,$}
\begin{equation}\label{eq:}
 \Re\left\{\frac{(1-\lambda)\delta^{\alpha}_{_{n}}f(z)+\lambda z[\delta^{\alpha}_{_{n}}f(z)]'}z\right\}>\beta,z\in U,n\in N_{0},0\leq\beta<1, \lambda\geq1.
\end{equation}

and

\begin{equation}\label{eq:}
 \Re\left\{\frac{(1-\lambda)\delta^{\alpha}_{_{n}}g(w)+\lambda w [\delta^{\alpha}_{_{n}}g(w)]'}w\right\}>\beta,w\in U,n\in N_{0},0\leq\beta<1, \lambda\geq1,
\end{equation}
\end{Definition}
where the function $g(z)$ defined by (2).

\ \\

\begin{thm}.
Let $f (z)$ given by (1) be in the class $H_{\Sigma}(\beta,\mu,\lambda), 0\leq\beta<1, \mu\geq0,$ and $\lambda\geq1.$ Then
\begin{equation}\label{eg:}
|a_{2}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-2 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-2 \\ k-2\end{array}} \right ) } \end{array}\right]\sqrt{\frac{2(1-\beta)}{1+2\lambda}}\end{equation}
\begin{flushleft}
and
\end{flushleft}

\begin{equation}\label{eg:}
    |a_{3}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-3 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-3 \\ k-3\end{array}} \right ) } \end{array}\right]\left[\frac{4(1-\beta)^{2}}{(1+\lambda)^{2}}+
    \frac{2(1-\beta)}{(1+2\lambda)}\right].
\end{equation}
\end{thm}

\begin{proof}.
It follows from (34) and (35) that there exists $p,q\in P$ such that
\begin{equation}\label{dlabel}\frac{{(1-\lambda)\delta^{\alpha}_{_{n}}f(z)+\lambda z [\delta^{\alpha}_{_{n}}f(z)]^{'}}}{z}=\beta+(1-\beta)p(z),\end{equation}

and
\begin{equation}\label{dlabel}\frac{{(1-\lambda)\delta^{\alpha}_{_{n}}g(w)+\lambda w [\delta^{\alpha}_{_{n}}g(w)}]^{'}}{w}=\beta+(1-\beta)q(w),\end{equation}

\begin{flushleft}
where $a_{1}=1$, and have the forms

\begin{equation}\label{eq:}
p(z)=1+p_{1}z+p_{2}z^{2}+p_{3}z^{3}+.....\ \ ,
\end{equation}
and
\begin{equation}\label{eq:}
q(w)=1+p_{1}w+q_{2}w^{2}+q_{3}w^{3}+.....\ \ ,
\end{equation}
 respectively. Equating coefficients in (38) and (39) yields
\end{flushleft}
\begin{equation}\label{eg:}
    [(1+\lambda)A_{2}a_{2}=(1-\beta) p_{1},
\end{equation}
\begin{equation}\label{eg:}
        [(1+2\lambda)A_{3}a_{3}=(1-\beta)p_{2},
\end{equation}
\begin{equation}\label{eg:}
-    [(1+\lambda)A_{2}a_{2}=(1-\beta) q_{1},
\end{equation}
and
\begin{equation}\label{eg:}
        (1+2\lambda)[2A_{2}^{2}a^{2}_{2}-A_{3}a_{3}]=(1-\beta)q_{2}.
\end{equation}

From (42) and (44), we have

\begin{equation}\label{eg:}
-p_{1}=q_{1}\end{equation}
and
\begin{equation}\label{eg:}
            2(1+\lambda)^{2}A_{2}^{2}a^{2}_{2}=(1-\beta)^{2}(p^{2}_{1}+ q^{2}_{1}).
\end{equation}
Also, from (43) and (45), we find that
\begin{equation}\label{eg:}
            2(1+2\lambda)A_{2}^{2}a^{2}_{2}=(1-\beta)(p_{2}+ q_{2}),
\end{equation}
\begin{equation}\label{eg:}
|a^{2}_{2}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-2 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-2 \\ k-2\end{array}} \right ) } \end{array}\right]\frac{(1-\beta)(|p_{2}|+|q_{2}|)}{2(1+2\lambda)},\end{equation}

 \begin{flushleft}
 $\Rightarrow$
 \end{flushleft}
\begin{equation}\label{eg:}
|a_{2}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-2 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-2 \\ k-2\end{array}} \right ) } \end{array}\right]\sqrt{\frac{2(1-\beta)}{1+2\lambda}},\end{equation}
which is the bound on $|a_{2}|$ as given in (36).

Next, in order to find the bound on $|a_{3}|$ by subtracting
(45) from (43), we obtain

\begin{center}
    $ 2A_{3}(1+2\lambda)a_{3}=$
    \end{center}
\begin{center}
    $2(1+2\lambda)A_{2}^{2}a^{2}_{2}
    +(1-\beta)(p_{2}-q_{2})$

\end{center}

or, equivalently

\begin{center}
    $ a_{3}=\frac{2(1+2\lambda)A_{2}^{2}a^{2}_{2}}{2A_{3}(1+2\lambda)}$
  $ +\frac{(1-\beta)(p_{2}-q_{2})}{2A_{3}(1+2\lambda)}.$
    \end{center}

Upon substituting the value of $a_{2}^{2}$
from (47), we obtain

\begin{center}
   $ a_{3}=A_{3}\left[\frac{(1-\beta)^{2}(p^{2}_{1}+q^{2}_{1})}{2(1+\lambda)^{2}}+
    \frac{(1-\beta)(p_{2}-q_{2})}{2(1+2\lambda)}\right]$.
\end{center}

Applying Lemma 1.1 for the coefficients $p_{1},p_{2},q_{1}$  and $q_{2}$  we obtain
\begin{center}

   $ a_{3}=A_{3}\left[\frac{4(1-\beta)^{2}}{(1+\lambda)^{2}}+
    \frac{2(1-\beta)(p_{2}-q_{2})}{(1+2\lambda)}\right].$
\end{center}
\begin{center}

    $|a_{3}|\leq\left[\begin{array}{c}\frac { \left ( {\begin{array}{c} k+\alpha-1\\ k-3 \end{array}} \right ) }
{ \left ( {\begin{array}{c} k+\alpha-3 \\ k-3\end{array}} \right ) } \end{array}\right]\left[\frac{4(1-\beta)^{2}}{(1+\lambda)^{2}}+
    \frac{2(1-\beta)}{(1+2\lambda)}\right].$
\end{center}

which is the bound on $|a_{3}|$ as asserted in (37).
\end{proof}
\  \\
\begin{remark}1.
\textit{  For all $\alpha\geq0$, and $k=n$ in Theorems 2.2, we obtain the corresponding results due to Zhigang and Qiuqiu \cite{Zhigang}
}\end{remark}

\begin{remark}2.
\textit{  For all $\alpha\geq0$, and $k=n$ in Theorems 3.2 and 4.2, we obtain the corresponding results due to Frasin and Aouf \cite{Frasin}.
}\end{remark}

redpajama_set_name: RedPajamaArXiv


text:
Full-Airframe Sensing Technology for Hypersonic Aerodynamics Measurements
Professor Karen Willcox and Alumnus Michael Watkins Elected to National Academy of Engineering February 9, 2022
The National Academy of Engineering (NAE) announced today that Karen Willcox, professor in the Department of Aerospace Engineering and Engineering Mechanics and director of the Oden Institute for Computational Engineering and Sciences and Al Bovik, professor in the Department of Electrical and Computer Engineering at The University of Texas of Austin, have been elected to the […]
Noel Clemens Wins 2022 AIAA Aerodynamic Measurement Technology Award February 8, 2022
Professor Noel Clemens has been selected to receive the 2022 AIAA (American Institute of Aeronautics and Astronautics) Aerodynamic Measurement Technology Award. The award, established in 1995, is presented annually to a researcher who has exhibited continued contributions and achievements toward the advancement of advanced aerodynamics flowfield and surface measurement techniques for research in flight and ground test applications. […]
Jayant Sirohi Named Technical Fellow of Vertical Flight Society September 8, 2021
Jayant Sirohi, a professor in the Department of Aerospace Engineering and Engineering Mechanics, has been named a Technical Fellow of the Vertical Flight Society (VFS) for 2021. The society, which was originally established as the American Helicopter Society in 1943, is the world's oldest and largest technical society dedicated to the understanding and advancement of […]
Julie Pham Recognized with Aviation Week Network's 20 Twenties Program Award August 2, 2021
Aerospace engineering graduate student Julie Vi Pham is one of only 20 students across the globe named to Aviation Week Network's 20 Twenties Class of 2021. Winners are selected not only for their academic performance, but also for their ability to communicate the value of their research and to contribute to a broader community. According to […]
New NASA-UT Hypersonics Project Aims to Transform Sensing for High-Speed Vehicles December 14, 2020
NASA and the Air Force Office of Scientific Research are backing a team of four universities, led by The University of Texas at Austin, in a project to redefine sensing and analysis of hypersonic vehicles, which can travel at least five times the speed of sound and potentially revolutionize space and air travel. The three-year, […]
Noel Clemens
clemens@mail.utexas.edu
© 2023 FAST

redpajama_set_name: RedPajamaCommonCrawl


The first thing you notice when skipping trough the book is that it is very nicely designed. It has all full color images, nice font and a well thought of structure.
The first few chapters are about project (server and Project Online) in general, a necessity in all Microsoft Project books if you ask me. However, there is one paragraph I would advice anyone to read: paragraph 2.4. Go to your local book store and read that paragraph if nothing else. It concerns the project scheduling engine, and is very well written.
Moving forward into the book we get a glimpse at the Sensei Project Solutions offering called "Proactive PPM". Exercises in the book refer to this environment, and the reporting module in particular looks awesome. The structure that Sensei has introduced into the environment consists of 6 major area's and is well thought of and would help any organization structure their project management efforts.
I give the book "Proactive PPM with Microsoft Project 2013": 5 out of 5 stars.
Buy it if you are in the USA and looking for a great PPM implementation partner but can't choose. Buy it if you're not in the US, and go right to the download page to get the exercises (and don't forget paragraph 2.4).
Did you like reading the review? There is more; check out the other reviews I did on the book reviews page. Do you have a book that you like reviewed on my blog, let me know. Also, consider following the blog to get the free custom UI ribbon I discuss in another post.


text:
Jarrett Fuller
Andrew Garfield as Jonathan Larson in tick, tick...Boom!
They'll Tell the Story of Tonight
tick, tick…Boom!, the new Netflix film and directorial debut of Lin-Manuel Miranda, is an adaptation of Jonathan Larson's small musical-slash-one-man show of the same name. Miranda, of course, is known as the man behind the Broadway success Hamilton and Larson, a prodigy in his own right, is known for writing another Broadway smash hit: Rent. I enjoyed the film, overall: Andrew Garfield embodies Larson perfectly and the ensemble cast does a wonderful job bringing the music (and 1980s bohemian New York) to life.
Unlike Miranda, Larson never saw the success of his Broadway show. He died unexpectedly the night before the first cast reading of an undiagnosed aneurysm at 35. tick, tick…Boom! is a decidedly smaller production than the other work both Miranda and Larson are known for. "tick, tick…Boom!" is an autobiographical show about a character also named Jonathan, who, about to turn thirty, wonders if he'll ever make it as an artist and musician. The plot follows Jonathan as he tries to stage a complicated and confusing sci-fi musical before entering his new decade, while balancing his work as a waiter at a New York diner. Miranda smartly bounces back and forth between a faux-stage production of the show and scripted interludes that flesh out Larson's life and process. It's fast moving, anchored by Larson's catchy show tunes, while also being intimate and personal, staging one artist's life against a backdrop of 1980s New York and the AIDS crisis.
Miranda is well documented in his admiration for Larson and for Rent and tick, tick…Boom!is a show that makes sense for Miranda to choose as his directorial debut: it's a niche Broadway show and Miranda is a product of Broadway. It's a semi-autobiographic musical and Miranda made a name for himself first with his own semi-autobiographical, In The Heights. It's a story about art and life, ambition and failure, legacy and death. In other words, it's what all of Miranda's work is about.
I've always found Miranda's interested in legacy fascinating. His stories are about people (usually men) with big ambitions and big dreams. (There's a million things I haven't done, but just you wait.) They want to be remembered by history. (They'll tell the story of tonight.) Hamilton is often talked about as a story of America's founding but I've always been drawn to the personal story embedded inside it: the story of an ambitious writer trying to balance work with his young family, of wanting to be remembered in history, sometimes at expense of the present.
The core of Hamilton, in my view, is this verse from Eliza, his new wife, after she tells Alexander that she is pregnant:
We don't need a legacy
We don't need money
If I could grant you peace of mind
If you could let me inside your heart…
Oh, let me be a part of the narrative
In the story they will write someday
Let this moment be the first chapter:
Where you decide to stay
And I could be enough
And we could be enough
That would be enough
This is Hamilton's core tension and these lines would fit right at home inside tick, tick…Boom! as well. Miranda expands the love story in the film with Susan, Larson's girlfriend, who gets a job upstate (Another parallel: Hamilton moves uptown!) and wants Jonathan to come with her. He keeps putting off the conversation, putting the work ahead, trying to stage his show. The opening lines of tick, tick…boom! are about the dread of turning thirty while still unable to create art of value: Stop the clock / Take time out / Time to regroup / Before you lose the bout. I'm again reminded of a Hamilton: Why do you write like you're running out of time?
Miranda's characters are ambitious, hard-working, creative, and sometimes myopic and Miranda, too, is clearly ambitious. And his work is laced with this rush to produce. His first show, In the Heights, debuted when he was only 27. His output has only increased since Hamilton, writing songs for Disney movies, producing and acting, and other film and music work. Perhaps Miranda is thinking about his legacy too. It's a narrative I know all too well and is, perhaps, the reason I find Miranda's body of work so compelling.
"It seems to be that shared sense of determination between Miranda and Larson that makes Miranda's Tick, Tick…Boom! feel so tender, so affectionate: You're able to empathize utterly with Larson's fears of running out of time because Miranda understands them so well," writes Constance Grady in Vox. "Under Miranda's direction, the film becomes a tribute to ambition itself, to the panic of being young and talented and striving but not quite getting there yet."
A few unordered thoughts on design school critique
Five Years and 200 Episodes of Scratching the Surface
Jarrett Fuller is a designer, writer, educator, and podcaster. RSS feed.
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Regional Events Calendar
Gumby Trail Runs
January 29, 2022 8:00 am - 11:30 am Granite Beach-Folsom Lake SRA, 8000 Douglas Blvd, Granite Bay, United States + Google Map
> View Details
Jed Smith Ultras
February 5, 2022 7:30 am - 4:00 pm American River Parkway – Watt Ave. River Access Park, 8713 La Riviera Dr., Sacramento, United States + Google Map
50 Mile / 50K / 30K / Half Marathon
San Francisco Half Marathon/10K/5K
February 6, 2022 8:00 am - 1:00 pm Golden Gate Park, Martin Luther King Drive at Bernice Rogers Way, San Francisco, United States + Google Map
Half Marathon / 10K / 5K
February 12, 2022 8:00 am - 11:30 am Country Club Plaza, 2310 Watt Ave, Sacramento, United States + Google Map
4 Mile Timed Run / 1.8 mile untimed walk.
February 20, 2022 Playfields Park, 2500 Research Park Dr, Davis, United States + Google Map
The 39th Annual Davis Stampede will take place on Sunday, February 20, 2022.
Surfer's Path 10K & 5K
February 27, 2022 8:00 am - 12:00 pm Santa Cruz – 41st Ave, 808 41st Avenue, Santa Cruz, United States + Google Map
10K/5K
March 6, 2022 7:00 am - 4:00 pm Vintage High School, 1375 Trower Ave, Napa, United States + Google Map
Marathon / Half Marathon / 5K
March 12, 2022 8:00 am - 11:30 am Raley Field, 400 Ballpark Dr, West Sacramento, United States + Google Map
5K / 10K / Kids run
March 13, 2022 7:30 am - 12:30 pm Raley Field, 400 Ballpark Dr, West Sacramento, United States + Google Map
March 20, 2022 7:00 am - 2:00 pm Snow Park, Harrison Street & 19th Street, Oakland, United States + Google Map
Marathon / Half Marathon / 10k / 5K
March 26, 2022 Community Park, Corner of Covell Blvd. and F Street, Davis, United States + Google Map
The Lucky Run will take place on Saturday, March 26, 2022 and offer 5K, 7K and 10K distances, plus a kids fun run.
Modesto Marathon / Half Marathon / 5K
March 27, 2022 7:00 am - 3:00 pm N and 11th Streets, N Street at 11th Street, Modesto, United States + Google Map
Marathon / Half / Relay / 5K / Kids Mini Marathon
Wildflower Run
March 27, 2022 8:30 am - 11:30 am Live Oak High School, 1505 East Main Avenue, Morgan Hill, United States + Google Map
10K / 5K/ 2K
Credit Union SACTOWN Run
April 3, 2022 7:30 am - 12:00 pm Capitol Mall at 7th Street, Capitol Mall at 7th Street, Sacramento, United States + Google Map
5K / 10 Mile
April 24, 2022 7:30 am - 11:30 am Gate 12 Parking – Alameda County Fair, Rd. 12, Valley Ave,, Pleasanton, United States + Google Map
The Pleasanton Run for Education offers a family-friendly race from the Alameda County Fairgrounds through downtown Pleasanton.
IPA 10K
April 29, 2022 - April 30, 2022 The Barlow Market District, 1670 McKinley St., Sebastopol, United States + Google Map
10K and 3K
Parkway Half Marathon and 5K
April 30, 2022 7:00 am - 2:00 pm William Pond Park, 5700 Arden Way, Carmichael, United States + Google Map
Half Marathon / 5K
Surfer's Path Half Marathon
May 22, 2022 7:00 am - 12:00 pm Santa Cruz Beach – 400 Beach St., 400 Beach Street, Santa Cruz, United States + Google Map
July 9, 2022 7:00 pm - 11:00 pm 201 Cousteau Place, 201 Cousteau Place, Davis, United States + Google Map
This is a fun and festive evening event replete with lots of cool glow in the dark themed race items, an energetic atmosphere and great running/walking routes.
Wahine 10K/6K
October 16, 2022 8:00 am - 12:00 pm Capitola Village, 203 Esplanade, Capitola Village - Corner of Esplanade & San Jose Ave., United States + Google Map


I don't say that lightly. It is against my nature to disparage another's character.
But I can come to no other conclusion.
You are the one who, as a Senator, charged with doing the business of the country, of keeping in mind the common good, publicly divulged in 2009 that your primary legislative goal was to make sure that Barack Obama was a one-term president.
Do you understand that words mean things? Do you understand that to name something a catastrophe is to judge it not only an abject failure, but that it has done irreparable harm? Hurricane Katrina was a catastrophe. The tsunami that hit the Japanese mainland in 2011 was a catastrophe.
The Affordable Care Act now has over 7 million sign-ons. How many of those have health insurance for the first time won't be known for several weeks. Still, even by the most conservative and critical estimates, millions of people who previously did not have health care coverage now do. We have finally begun to catch up with the other developed nations when it comes to making sure that every one of our citizens has access to healthcare. And to make sure that the cost of the healthcare is evenly distributed.
Now Sen. McConnell, you may not agree with the methodology. You may wish it had come down differently. Frankly, I agree with you. i don't think this is the be-all, end-all. I wish it had been crafted differently. Still, for all that I disagree with, this is a major step forward.
So how is it a catastrophe? Because it wasn't sponsored by your party? Because it doesn't push forward your own personal, get-reelected agenda?
I ask you this question in particular because, for all of your blathering about what's wrong with the Affordable Care Act, neither you nor your party offered any alternative.
And since it appears that you have no interest in a rational dialogue about this issue, but only that you wish to cast aspersions on your opponent — in this case, President Obama and his clearly successful Affordable Care Act — I can come to no other conclusion than that you are a demagogue.
As a citizen of this great country, one who looks beyond party affiliation to our common good, I say, shame on you.
This entry was posted in Uncategorized and tagged Affordable Care Act, Common Good, Mitch McConnel, Obamacare on April 1, 2014 by Jim Honig.
Thanks, Larry. I read your comment in my email inbox and laughed out loud!
With this sort of continuing vitriolic political rhetoric coming from our elected officials is it any wonder citizens are scathing in their views of national debate? This is so far out of the public square of coversation. It seems now almost to be good for nothing else than shock value.
Yep, Paul. Although, not even shock value. Partisanship with neglect for the larger good.


NewTek Discussions > TriCaster > TriCaster Classifieds > Services & Resumes > Sacramento area?
View Full Version : Sacramento area?
Hey, anybody out there in the Sacramento area (Rancho Cordova specifically)? I'm flying in for a production next week, and I may need to beg/borrow/rent some gear, even if it's just a few computer monitors or somethin'. PM me or email me at [email protected] Thanks.
Hit up Ted Ruiz, he should be able to help you. He is somewhat close by.
:) you know me so well.
Sorry I missed this. You have mail. We're not that far away.


text:
Home | Blog | About | Contact | Women in Science Bookstore
View of Marie Curie in 1927
Jenny F. Scientist has an interesting post on the profile of Marie Curie in Benjamin Harrow's Eminent Chemists of our Time, published in 1927. As she points out, the biography starts out positively, pointing out that Curie was not receiving the recognition she deserved:
The foremost scientist of France, and the greatest woman scientist in the history of mankind, [Curie] counts politically less than many a man fit for the lunatic asylum. And as if to encourage that conception of women to which so many men cling tenaciously, the French Academy, numbering among its members the élite of French intellect, decide [sic] that woman, be she ever so much a genius, cannot be admitted into their sanctum. If further proof were needed that intellect often runs counter to freedom, and that scientists who work so strenuously for an enlargement of their scientific horizon often belong to the most reactionary group in politics, the case of Madame Curie affords an excellent example.
As it goes on, it's clear that Curie is held out as an exception - a woman "as good as a man" at science. Not only that, but there is a whole paragraph reassuring the reader that Curie hasn't let her feminine duties lapse:
Mme. Curie may be the great scientist, but she has many of the traits of femininity and motherhood which most men of all ages have admired. Aside from her work, her attention is devoted almost exclusively to the welfare of her two daughters... When the two children were younger Mme. Curie made all their dresses, and washed and ironed the more delicate pieces of lingerie.
As Jenny points out, this really isn't "history".
This wouldn't be quite so distressing if these attitudes were, y'know, gone. Women have to work twice as hard to get recognition? Check. Given lesser positions for equal work? Excluded from Old Boys' Club? Check. It's tradition? Check. 'Don't worry, science doesn't make her completely unwomanly, she still cooks and cleans and dresses pretty'? CHECK.
Looking at profiles of current women scientists, I've noticed many that make a point of including personal tidbits that demonstrate "typical" femininity - time spent with the children, hobbies such as cooking or sewing, and the like. While none of those things are bad - even scientists have interests outside of their work - it's annoying that such facts are typically omitted from the profiles of male scientists. It simply reinforces the attitude that science is an inherently non-feminine activity and that women in science need to demonstrate that they have feminine "credentials" by their activities outside the workplace. I'm hoping that 80 years from now profiles of male and female scientists won't be noticeably different in their content.
Categories: life as a woman scientist, physics, pioneers, stereotypes
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After more than 5 years of development, the release of Cheetah 7.0 without doubt, is the biggest Upgrade in the history of Cheetah3D. Version 7 doesn't just add tons of new features but also big parts of its core have been rewritten and modernized. As a result, Cheetah3D is leaner and faster than ever while offering many new powerful features.
The biggest new feature in v7.0 is the addition of the new unbiased render engine (Falcon) which will build the rendering foundation for the coming years. But also the new Boolean (CSG) operations greatly improve Cheetah3D and make it an even better companion app for people interested in 3D printing.


I'm checking out a 2012 67 strada, and let me say Rossi has been amazing at corresponding w me and making setup suggestions!!
I think the size chart is now more accurate on the new layup. My buddy and I have 2011's and both prefer the next size up on the 2012 Strada.
I have a 68" 2012 Strada. Is that the correct size for me? I ski at 34mph, 28off (ish) and am 185lbs.
I haven't had a chance to try a 67".
I like the 67" Strada 2011, ski 28-35 at 34 (on a good Day). currently weigh 195. will probably upgrade to a 2012 model in the next couple of months. At 5'almost7" tall I feel 68" skis are to big and I have trouble in the turns with them.
@Laz They say you want to ride the biggest ski that you can turn and the 2012 does turn better than the 2011. It's tough to make any reccomendations without seeing you ski but with your weight and line the 68"could work. 35 off and up probably the 67". If you have the chance to ski both then you can be the judge.


Angiostrongylus cantonensis has been the only parasite among Angiostrongylidae to cause human central nervous system infection characterized by eosinophilic meningitis or meningoencephalitis. The mechanism of the extensive neurological impairments of hosts caused by A. cantonensis larvae remains unclear. The aim of the present study was to investigate apoptosis, necroptosis and autophagy in the brains of mice infected with A. cantonensis, which will be valuable for better understanding the pathogenesis of angiostrongyliasis cantonensis.
Functional and histological neurological impairments of brain tissues from mice infected with A. cantonensis were measured by the Morris water maze test and haematoxylin and eosin (H&E) staining, respectively. The transcriptional and translational levels of apoptosis-, necroptosis- and autophagy-related genes were quantified by quantitative real-time polymerase chain reaction (RT-PCR), and assessed by western blot and immunohistochemistry (IHC) analysis. Apoptotic and necroptotic cells and their distributions in infected brain tissues were analysed by flow cytometry and transmission electron microscopy (TEM).
Inflammatory response in the central nervous system deteriorated as A. cantonensis infection evolved, as characterized by abundant inflammatory cell infiltration underneath the meninges, which peaked at 21 days post-infection (dpi). The learning and memory capacities of the mice were significantly decreased at 14 dpi, indicating prominent impairment of their cognitive functions. Compared with those of the control group, the mRNA levels of caspase-3, -4, -6, and RIP3 and the protein levels of caspase-4, cleaved caspase-3, cleaved caspase-6, RIP3, and pRIP3 were obviously elevated. However, no changes in the mRNA or protein levels of FADD, Beclin-1 or LC3B were evident, indicating that apoptosis and necroptosis, but not autophagy, occurred in the brain tissues of mice infected with A. cantonensis. The quantitative RT-PCR, western blot, IHC, flow cytometry and TEM results further revealed the apoptotic and necroptotic microglia, astrocytes and neurons in the parenchymal and hippocampal regions of infected mice.
To our knowledge, we showed for the first time that A. cantonensis infection causes the apoptosis and necroptosis of microglia and astrocytes in the parenchymal and hippocampal regions of host brain tissues, further demonstrating the pathogenesis of A. cantonensis infection and providing potential therapeutic targets for the management of angiostrongyliasis.
Angiostrongylus cantonensis is the most common cause of eosinophilic meningitis worldwide. As accidental hosts, humans can become infected via the ingestion of undercooked intermediate hosts (Pomacea canaliculata, Achatina fulica, etc.) or contaminated water or food that contains third-stage larvae (L3) [1, 2]. After penetrating the intestinal wall, A. cantonensis migrate in the body through the bloodstream, finally passing the blood-brain barrier to further develop in the central nervous system (CNS). Larvae in the brain tissue cause direct mechanical damage and severe inflammation, resulting in eosinophilic meningitis or encephalitis. In addition to the cerebrum and meninges, the cerebellum, brainstem and spinal cord can be affected. Clinical symptoms, manifested as CNS injuries, include severe headache, neck stiffness, convulsions and nausea .
Parasitic infections of the CNS include protozoans (Plasmodium, Trypanosoma cruzi, Toxoplasma gondii and amoebae) and metazoans (Schistosoma, Paragonimus, larval stages of Taenia solium, Echinococcus granulosus, Spirometra mansoni, and A. cantonensis), and the pathogenesis of these neuroparasites include the apoptosis and necroptosis of host cells . The major pathogenetic mechanism of cerebral amebiasis lies in the killing of mammalian cells by trophozoite-induced apoptosis . Disruption of the endothelium via apoptosis leads to the leakage of red blood cells, ring haemorrhage, and activated coagulation in adjacent nervous tissue in cerebral malaria . In neurocysticercosis, neurological deficits, particularly learning and memory deficits, are generated by the extensive and significant apoptosis of hippocampal cells  and apoptosis of CD3+ T lymphocytes in the brains of hosts induced by T. solium cysticerci may be a mechanism by which the parasite downregulates its host's cellular immune response during early cysticercosis . The most common presentation of cerebral toxoplasmosis in HIV-infected patients is mass lesions consisting of well-defined areas of coagulative necroptosis with or without haemorrhage . The gross appearance of tumoural lesions in neuroschistosomiasis is characterized by the presence of necrotic-exudative granuloma containing eggs surrounded by necrotic and elongated epithelioid cells .
Although A. cantonensis is the most common cause of eosinophilic meningitis worldwide, the major cell populations and cell injuries in the host brain after infection are not entirely clear . To further reveal the pathogenesis of angiostrongyliasis cantonensis in this study, the Morris water maze test was used to test the neural functionality of A. cantonensis-infected hosts. Quantitative RT-PCR, western blot and immunohistochemistry (IHC) analyses were combined to detect apoptosis, necroptosis and autophagy in mouse cerebral parenchymal and hippocampal cells. Flow cytometry and transmission electron microscopy (TEM) were performed to evaluate the cell death of parenchymal and hippocampal astrocytes, neurons and microglia.
Female BALB/c mice (6–8 weeks old) were purchased from Guangdong Medical Laboratory Animal Center and housed in a specific pathogen-free environment and had unlimited access to food and water.
One batch of mice was randomly divided into 6 groups (9 mice per group) and orally infected with A. cantonensis third-stage larvae (L3, 30 per mouse), except for the normal controls. Groups were named according to the number of day(s) post-infection (dpi): group G1 (uninfected mice), group G2 (mice infected for 1 day), group G3 (mice infected for 3 days), group G4 (mice infected for 7 days), group G5 (mice infected for 14 days) and group G6 (mice infected for 21 days). Brain samples from each group were prepared for mRNA and protein extraction or fixed for immunohistochemistry analysis. Animals were euthanized under deep anaesthesia by ether inhalation followed by blood-letting.
Another batch of mice was used for studying neurological function, flow cytometry analysis and transmission electron microscopic observation. They were divided into 4 groups and orally infected with 30 L3 for 7, 14 and 21 days or not infected (control group). After neurological function evaluation, flow cytometry analysis of brain tissues was carried out. Brain tissues from the 0 dpi and 21 dpi groups were subjected to transmission electron microscopy.
All the infectious A. cantonensis L3 used in this study were obtained from Biomphalaria glabrata 21 days after infection of the first-stage larvae (L1) of the parasite. The snails were homogenized and digested in a pepsin-HCl solution (pH 2.0, 500 IU pepsin/g tissue) at 37 °C in an incubator for 40 min. Then, infectious L3 were washed in PBS and counted under an anatomical microscope for animal infection .
The Morris water maze test was used as described in a previous study  to compare learning and memory skills between normal and infected mice. The water maze consisted of a large, circular tank (180 cm in diameter × 60 cm high) filled with water (22 ± 1 °C). A stationary platform was hidden 1.5 cm below the water surface, and white paint was added to make the platform invisible. During cued training, mice were placed into the pool four times each training day (days 1, 2 and 3), once from each of the four quadrants, and then required to find the platform. Animals that located the platform were allowed to rest for 30 s; those that failed to find the platform within 60 s were gently guided to the platform to rest for 30 s. Escape latency, or the time required to reach to the platform, was recorded for each mouse (day 4), and place navigation was used to evaluate their learning and memory skills. The spatial probe test, used to evaluate mouse memory retention, was performed on day 5. The platform was removed, and the probe task was performed in the third quadrant. The swim escape latency, average swim speed, time spent in the target quadrant, and number of times the mice crossed the previous location of the platform were recorded by a video tracking system (Taimeng Tech, Chengdu, China).
Mice brains were collected at 0, 1, 3, 7, 14 and 21 dpi, fixed in 4% paraformaldehyde and embedded in paraffin. Brain sections were then de-paraffinized in xylene, rehydrated via graded alcohols and stained with H&E (Biosharp, Wuhan, China) according to the manufacturer's protocol. Pathological changes were observed under an inverted microscope (Leica, Heidelberg, Germany).
Total mouse brain RNA was extracted using TRIzol® Reagent (Thermo Fisher Scientific, Waltham, USA) according to the manufacturer's protocol, and RNA yield and purity were determined by the NanoDropTM spectrophotometer (Thermo Fisher Scientific). The first cDNA strand was synthesized at 42 °C for 1 h using the RevertAid First Strand cDNA Synthesis Kit (Thermo Fisher Scientific).
For RT-PCR, primers for detecting cell death genes were designed using AlleleID software. The sequences of the target genes and that of the internal control β-actin gene are listed in Table 1. RT-PCR was performed with SYBR® Premix Ex Taq™ (TaKaRa, Dalian, China) in a volume of 20 μl. PCR samples were preheated to 95 °C for 30 s, followed by 40 cycles of 95 °C for 5 s and 60 °C for 20 s. The melt curve was then created by heating at 95 °C for 1 s, 65 °C for 15 s, and 55 °C for 30 s. Reactions were performed on the LightCycler480® Real-Time PCR System (Roche Diagnostics, Reinach, Switzerland), and experiments were repeated three times as independent biological replicates. The mRNA levels of these genes were measured by the Ct value (threshold cycle), and the relative expression levels were calculated with the 2-ΔΔCt method .
Total mouse brain proteins were extracted using Western-IP Lysis Buffer (Beyotime,Wuhan, China) and quantified using the BCA protein assay kit (Beyotime, Wuhan, China). In total, 10 μg of total proteins were electrophoresed on 12% SDS polyacrylamide gels and transferred onto nitrocellulose membranes. The membranes were blocked with PBS/Tween 20® (PBST) containing 5% non-fat milk for 90 min at room temperature and then incubated overnight at 4 °C with the following primary antibodies: anti-caspase-3, anti-cleaved caspase-3, anti-caspase-6, anti-cleaved caspase-6, anti-RIP3, anti-Beclin-1 (Cell Signaling Technology, Danvers, USA), anti-caspase-4, anti-phosphor-RIP3 (Abcam, Cambridge, UK), anti-LC3B (Beyotime,Wuhan, China), and anti-β-actin (Cell Signaling Technology, Danvers, USA) as the control. After incubation with HRP-conjugated goat anti-rabbit IgG or HRP-conjugated goat anti-rat IgG (Cell Signaling Technology), the nitrocellulose membranes were washed three times, and bands were visualized by chemiluminescence with Pierce Enhanced Chemiluminescence Detection Reagent (Millipore, Burlington, USA) on the ChemiDoc™ Touch imaging system (Bio-Rad, Hercules, USA). Relative band intensity was analysed by AlphaViewTM software (Alpha Innotech Corporation, San Jose, USA).
Mouse brains were isolated, fixed in 4% paraformaldehyde (PFA) overnight at 4 °C and embedded in paraffin. Then, the brain sections were de-paraffinized in xylene, rehydrated via a graded ethanol series, and subjected to antigen retrieval by boiling the slices in citrate buffer (pH 6.0) with high heat for 15 min and medium heat for 15 min in a microwave oven. For IHC analysis, sections were treated with 3% H2O2 for 10 min to remove endogenous peroxidase, blocked with 1% bovine serum albumin (BSA) in PBS (blocking solution) at room temperature for 1 h, and incubated with anti-caspase-3, anti-cleaved caspase-3, anti-caspase-6 (Cell Signaling Technology), anti-NeuN (Abcam) anti-RIP3 (ABclonal, Wuhan, China), or anti-LC3B (Beyotime) diluted in blocking solution at 4 °C overnight. After being washed 3 times in PBS, the sections were incubated with an HRP-conjugated secondary antibody (DAKO, Glostrup, Denmark) at room temperature for 30 min and then stained with 3, 3′-diaminobenzidine (DAB) for 15 s. Haematoxylin was used for cell nuclei detection. Stained sections were visualized and digitally scanned with an inverted light microscope (Leica).
Mice were euthanized, and their parenchymal and hippocampal tissues were separated, removed and collected into 5 ml of Dounce buffer (Hank's balanced salt solution containing 15 mM HEPES and 0.5 mM L-glutamine). The samples were homogenized on ice using a glass homogenizer, and the suspensions were pipetted onto a 70 μm cell strainer over a 15 ml conical tube and then centrifuged for 1 min at 1000× rpm at 4 °C. The pellets were resuspended in FACS buffer (0.5% BSA, 0.1% NaN3 and 25 mM HEPES in PBS) for single-cell suspension preparation. To increase the microglia yield, myelin was removed using Myelin Removal Beads II (Miltenyi Biotec, Bergisch Gladbach, Germany). Cells were blocked using Fc block prior to surface antibody staining at 4 °C for 30 min in the dark. In total, 2.5 μl of the following surface antibodies were used: Annexin V PE-Cyanine7, FVD eFluor 780 (eBioscience, Waltham, USA), CD45-BV421, and CD11b-BV711 (BD Biosciences, Franklin Lakes, USA). After a 20 min incubation, cell suspensions were fixed and permeabilized using fixation/permeabilization buffer (BD Biosciences) and intracellular antibodies (0.5 μl of NeuN-Alexa Fluor 488 and 2.5 μl of PE-conjugated GFAP in 50 μl of BD Perm/WashTM buffer) were then added. Cells were analysed on a CytoFLEX S flow cytometer (Beckman Coulter, Atlanta, USA), and 10,000 cells were collected per tube. Data analysis was performed using FlowJo software (Tree Star, San Carlos, USA).
After perfusion with fixatives, small cubes of the latero-ventral hippocampus and parenchymal layers were excised from the brains of normal and 21 dpi mice (n = 3 per group) and immediately fixed in 2.5% glutaraldehyde (v/v) in 100 mM phosphate buffer with 2% PFA (w/v) at 4 °C overnight. The cubes were post-fixed in 1% osmium tetroxide in 100 mM phosphate buffer for 1.5 h at room temperature. The samples were then washed, dehydrated in a graded series of ethanol (50, 70, 80, 90 and 100%), cleared in acetone and embedded in Eponate 12 resin (Ted Pella Inc., Redding, USA). Ultrathin sections (60 nm thickness) were cut with a diamond knife (Diatome, Nidau, Switzerland) on a Leica EM UC7 ultra-microtome, stained with a 2.0% uranyl acetate solution and a 2.0% lead citrate solution, and observed using a Tecnai G2 Spirit Twin electron microscope (FEI, Hillsboro, USA) operated at 80 kV.
Statistical analyses were performed using GraphPad Prism 5.0 (GraphPad Software, San Diego, USA) with two-tailed unpaired Student's t-test and SPSS 20.0 (IBM Corp., NY, USA) with one-way analysis of variance (ANOVA) followed by the Tukey-Kramer test. The data are presented as the means ± standard deviation (SD). Differences among comparisons were considered statistically significant for P-values less than 0.05.
During the 4 day place navigation test, significantly (F (3,20) = 60.19, P < 0.0001 and F (3,20) = 73.31, P < 0.0001, respectively) prolonged escape latency times and extended swimming distances were observed in the 14 dpi (44.65 ± 14.87 s and 362.89 ± 63.82 cm, respectively) and 21 dpi (59.5 ± 1.04 s and 692.49 ± 130.11 cm, respectively) groups compared with mice in the 0 dpi (7.93 ± 2.51 s and 88.31 ± 17.99 cm, respectively) and 7 dpi (12.76 ± 4.35 s and 150.86 ± 50.48 cm, respectively) groups. In addition, disparity in the above two parameters between the 14 dpi and 21 dpi groups was statistically significant (F (3,20) = 60.19, P = 0.019 and F (3,20) = 73.31, P < 0.0001, respectively) (Fig. 1a-c), while no significant differences in average swimming speed were observed between normal and infected mice (P > 0.05) (Fig. 1d). In the spatial probe test on day 5, no significant distinction among the groups in terms of platform area crossing were observed (P > 0.05) (Fig. 1e). However, mice in the 14 dpi (26.47 ± 9.37 s) and 21 dpi (42.93 ± 18.34 s) post-infection groups significantly extended their time spent in the target quadrant compared with the 0 dpi (6.97 ± 2.48 s) and 7 dpi (11.48 ± 5 s) groups (F (3,20) = 14.25, P < 0.0001), while no significant difference in the time spent in the target quadrant between the 21 dpi and 14 dpi groups was observed (P > 0.05) (Fig. 1f). The results indicated a clear time-dependent reduction in the learning and memory retention capacities of mice infected with A. cantonensis.
H&E staining reflected the histopathological injuries and inflammation of mouse brains infected with A. cantonensis. No histopathological injuries or inflammatory cells were observed in the brains of the 0 dpi and 1 dpi groups. After 3 dpi, a few inflammatory cells infiltrated into the mouse brains, aggregating on and thickening the meninges (black arrows). Worm transection in the infected parenchyma illustrated that this parasite could move into the brain after only 3 days of infection (red arrows). As the infection time extended, more inflammatory cells infiltrated into the mouse brains, and their histopathological statuses became more serious (Fig. 2).
To detect brain injuries in the infected mice, the mRNA levels of some molecules related to apoptosis, necroptosis and autophagy, including caspase-2, -3, -4, -6, -9, Cc, Smac, Bcl-2, Bad, Bcl-Xl, RIP3, FADD, Beclin-1 and LC3B, were measured. The mRNA levels of caspase-4, -6 and RIP3 in the infected mouse brains were 7-, 5- and 6-fold higher than those of normal mice. The mRNA levels of caspase-4, -6 and RIP3 increased as brain inflammation progressed, and the caspase-6 and RIP3 mRNA levels peaked and had statistical significance at 21 dpi (F (5,12) = 6.232, P = 0.0004 and F (5,12) = 8.755, P < 0.0001, respectively). The mRNA level of caspase-4 peaked at 14 dpi (F (5,12) = 6.386, P = 0.0051) (Fig. 3).
We next detected the expression levels of proteins associated with apoptosis, necroptosis and autophagy by western blot. Figure 4 shows obviously increased levels of the apoptotic proteins cleaved caspase-3 (F (5,12) = 80.86, P < 0.0001), caspase-4 (F (5,12) = 56.65, P < 0.0001) and cleaved caspase-6 (F (5,12) = 35.58, P < 0.0001) after A. cantonensis infection, and these levels peaked at 21 dpi, 7 dpi and 3 dpi, respectively. RIP3 expression was clearly upregulated from 14 dpi (F (5,12) = 8.458, P = 0.0009) to 21 dpi (F (5,12) = 8.458, P = 0.011) and peaked at 14 dpi. pRIPK3, an active mediator of necroptosis, was significantly elevated at 21 dpi (F (5,12) = 17.17, P < 0.0001). However, there was no significant effect on the expression levels of total caspase-3, total caspase-6 and Beclin-1 proteins compared to those of normal mice, and no clear accumulation of LC3B-II can be observed in the mice infected with the parasite (P > 0.05) (Fig. 4).
Caspase-3 and RIP3 expression in the parenchymal and hippocampal cells of the 0 dpi and 21 dpi groups were analysed by quantitative RT-PCR and western blot. A significant elevation in the RIP3 mRNA level after infection was observed, as it was 2- and 3-fold higher than those of normal mice in parenchymal (t (4) = 4.826, P = 0.017) and hippocampal cells (t (4) = 3.624, P = 0.0152), respectively. Furthermore, no obvious alterations of the caspase-3 mRNA level were observed (P > 0.05) (Fig. 5a). Western blot analysis showed a correspondingly significant elevation of RIP3 and pRIP3 expression in post-infectious parenchymal (t (4) = 9.374, P = 0.0007 and t (4) = 11.03, P = 0.0004, respectively) and hippocampal cells (t (4) = 9.139, P = 0.0008 and t (4) = 5.619, P = 0.0049, respectively). Similar conclusions were found regarding the cleaved caspase-3 protein levels in parenchymal cells (t (4) = 12.35, P = 0.0002) and hippocampal cells (t (4) = 7.3, P = 0.0019) (Fig. 5b, c). All data indicated that A. cantonensis infection could result in apoptosis and necroptosis in mouse hippocampal and parenchymal cells.
Expression and localization of caspase-3, cleaved caspase-3, caspase-6, RIP3, LC3B and NeuN were detected in the 0 dpi and 21 dpi groups by IHC. As shown in Figs. 6, 7, 8, cleaved caspase-3- and RIP3-positive cells were significantly increased in both parenchymal and hippocampal cells of the 21 dpi group. For cleaved caspase-3, the percentage of positive cells increased from 12.67 ± 3.06% to 51 ± 3.61% and 14 ± 4% to 55.33 ± 5.03% in the hippocampus and parenchyma, respectively. The number of RIP3-positive cells increased from 5.67 ± 1.53% to 54.33 ± 4.04% and 9.67 ± 2.08% to 88.33 ± 3.06% in the hippocampus and parenchyma, respectively. A mild elevation in the number of caspase-6-positive cells from 2 ± 1% to 23 ± 4.36% was observed in infected hippocampi, and no substantial changes were observed in the number of caspase-3-positive cells. Neither normal nor infected mouse brains exhibited LC3B-positive cells, implying that A. cantonensis infection does not lead to autophagy. Different infectious stages were then measured by similar procedures. The number of cleaved caspase-3-positive cells gradually multiplied from 1 dpi to 21 dpi and peaked at 58 ± 2.65% in parenchymal cells and 56 ± 5.29% in hippocampal cells at 21 dpi (Figs. 9 and 10). Parenchymal RIP3-positive cells peaked at 14 dpi at 82.67 ± 2.31%, while hippocampal RIP3-positive cells peaked at 21 dpi at 53.67 ± 5.51% (Figs. 9 and 10). The IHC results further proved that post-infectious apoptosis and necroptosis occur in mouse hippocampal and parenchymal cells.
Distinction between early-apoptotic cells and late-apoptotic/necrotic cells was detected by flow cytometry using the Annexin V PE-Cyanine7 and FVD eFluor 780 double-label staining technique. Proportions of late-apoptotic or necrotic parenchymal cells (Annexin V PE-Cyanine7+/FVD eFluor 780+) in the 14 dpi (48.9 ± 2.3%) and 21 dpi (22.25 ± 11.38%) groups were significantly increased compared with those in the 0 dpi (2.81 ± 1.27%) and 7 dpi (2.79 ± 1.88%) groups (Fig. 11). Notably, the late-apoptotic or necrotic cell counts peaked at 14 dpi (F (3,8) = 66.33, P < 0.0001), followed by a slight decline at 21 dpi in parenchymal cells. The latter still showed statistically significant distinction between the 0 dpi/7 dpi (F (3,8) = 66.33, P = 0.01) and 14 dpi groups (F (3,8) = 66.33, P = 0.002) compared with 21 dpi. Similarly, the proportions of late-apoptotic or necrotic hippocampal cells in the 14 dpi (3.58 ± 1.58%) and 21 dpi (25.05 ± 0.07%) groups were also significantly increased compared with those in the 0 dpi (1.09 ± 0.49%) (F (3,8) = 590.3, P = 0.032 and F (3,8) = 590.3, P < 0.0001, respectively) and 7 dpi (0.90 ± 0.06%) group (F (3,8) = 590.3, P = 0.023 and F (3,8) = 590.3, P < 0.0001, respectively). The late-apoptotic and necrotic cell counts in hippocampal cells peaked at 21 dpi, with a statistically significant difference from those of the 14 dpi group (F (3,8) = 590.3, P < 0.0001). Furthermore, no significant distinctions in early-apoptotic cell counts (Annexin V PE-Cyanine7+/FVD eFluor 780-) were found in any of the groups. The flow cytometry results revealed that apoptosis and necroptosis occur in hippocampal and parenchymal cells during A. cantonensis infection. The apoptotic and necrotic cell categories were further evaluated using different surface biomarkers (CD45 and CD11b for microglia, NeuN for neurons, GFAP for astrocytes). As indicated in Figs. 12 and 13, as the infection time extended, distinct elevations in the proportions of parenchymal and hippocampal astrocytes, neurons and microglia undergoing late apoptosis or necroptosis were observed, and almost 90% of the astrocytes and neurons had underwent apoptosis and necroptosis at 21 dpi.
Compared with the normal morphology and ultrastructure of cells in the 0 dpi group, the astrocytes (Figs. 14, 15f), microglia (Figs. 14g, 15k), oligodendrocytes (Fig. 15g) and neurons (Fig. 15h) of the 21 dpi group showed apparent swelling, rupture and loss of nuclear membrane integrity and visible swollen organelles (Fig. 15i), indicating that these cells underwent necrosis. Neuronal pyknosis and shrinkage (Figs. 14h, 15m) revealed that the neurons may have undergone apoptosis. Characteristics of apoptotic cells, such as patchy nuclear membranes, chromatin margination (Fig. 15l) and abnormally emerged smooth muscle cells (Fig. 15j), implied apoptosis and necroptosis of parenchymal and hippocampal cells. Hence, we concluded that significant morphological changes in hippocampal and parenchymal cells occur after A. cantonensis infection.
Eosinophilic meningitis or eosinophilic meningoencephalitis in humans is commonly caused by Angiostrongylus cantonensis, a food-borne zoonotic parasite, in southern Asia and the Pacific and Caribbean islands [14, 15]. The clinical symptoms of angiostrongyliasis cantonensis are characterized by severe headache, neck stiffness, paraesthesias and cranial nerve palsy [16, 17]. The neurological manifestations of neuroangiostrongyliasis include eosinophilic meningitis, encephalitis/encephalomyelitis, radiculitis and cranial nerve abnormalities, ataxia, tremors and paralysis, which have been observed in previous clinical reports [18–20] and in studies on infected experimental animal models [11, 21]. These characteristics coincide with our results that infected mice exhibited extensive brain injury and neurological disorder, as detected by the Morris water maze test (Fig. 1) and H&E staining (Fig. 2). However, the pathogenesis of A. cantonensis neurological dysfunction remains poorly understood. The tracks and microcavities caused by the migration of larvae in the brains of infected animals, as described in previous studies , cannot explain all the clinical neurological injuries in the hosts  or the distinct outcomes between permissive and non-permissive hosts after A. cantonensis infection since the same physical destruction of neural tissue caused by the migration of larvae can be seen within both of their brains . Interestingly, our previous  and the current findings indicate the obvious apoptosis and necroptosis of parenchymal and hippocampal astrocytes, neurons and microglia of mice infected with A. cantonensis (Figs. 3–10), which might provide new insights into the pathogenesis of neuroangiostrongyliasis.
The cell is the basic structural and functional unit of life. Cell death, as a natural process of life, plays an important role in the development and homeostatic balance of multicellular organisms [23–25]. According to morphology and molecular mechanisms, cell death is mainly divided into three categories: apoptosis, autophagy, and necroptosis (or necrotic cell death) . Apoptosis is an automatic and programmed process regulated by signalling pathways, including the death receptor signalling, mitochondria-mediated and endoplasmic reticulum stress pathways [27, 28]. All the pathways ultimately activate caspases to complete apoptosis. Caspase-3, -4, and -6 are important members of the caspase family , as their function in orchestrating apoptosis has been widely confirmed . In this study, we discovered that compared with those of uninfected mice, the caspase-4 and -6 mRNA levels and cleaved caspase-3, -4, and -6 expression levels of A. cantonensis-infected mice were elevated. As shown in Figs. 3 and 4, A. cantonensis infection could cause the apoptosis of mouse brain cells. Furthermore, qPCR, western blot, immunohistochemistry, flow cytometry and TEM analysis further proved that apoptosis mainly occurs in parenchymal and hippocampal astrocytes, neurons and microglia during A. cantonensis infection (Figs. 5–15). Although previous studies showed an elevation in the number of apoptotic leukocytes in post-infective parenchyma and subarachnoid space and the induction of apoptosis in endothelial cells and astrocytes after the addition of larvae extracts [31, 32], we observed for the first time in this study that A. cantonensis infection caused significant apoptosis amongst parenchymal and hippocampal astrocytes, neurons and microglia, which could partially account for the severe neural damage observed (Fig. 1). In addition, we first confirmed that the levels of RIP3 and pRIP3 increased as the infection time extended (Figs. 3, 4). RIP3 is the key to apoptosis and necroptosis and a specific marker for necroptosis . Thus, the increased RIP3 and pRIP3 levels indicated that A. cantonensis infection could induce the necroptosis of astrocytes, neurons and microglia (Figs. 5–15). Necroptosis is a recently recognized mechanism of programmed cell death that, unlike apoptosis, shows necrotic morphological changes with a patterned regulatory mechanism [34, 35]. Necroptosis can be induced by TNF-α, the activator of programmed cell death [36–38], and is mediated by its unique RIP3-dependent signalling pathway. In most cases, apoptosis and necroptosis co-exist, and a main difference between them is that necroptosis is accompanied by inflammation , causing inflammatory diseases, such as neurodegenerative disorders, haemorrhage-induced brain damage, Crohn's disease, multiple sclerosis and certain viral infections . Our study on A. cantonensis infection-induced brain apoptosis and necroptosis is not only consistent with our previous work in that the level of TNF-α, a trigger of apoptosis and necroptosis that is increased in the brains of mice infected with A. cantonensis , can be directly induced by the cystatin from A. cantonensis (unpublished data), but also further explains the pathogenesis of severe neural dysfunction accompanied with extensive eosinophilic CNS inflammation during A. cantonensis infection.
As the macrophages of the brain, microglia play both protective and toxic (damaging) roles in non-infectious pathological states, such as brain damage or neurodegenerative disorders [42, 43]. As the only immune cells in cerebral parenchyma, microglia are considered the first-line barrier protection for the CNS against pathogens (bacteria, viruses, parasites, etc.) [44–46]. Astrocytes are the most widely distributed cells in the mammalian brain and the largest population among glial cells . Thus, astrocytes play significant roles in survival functionality, neuronal development and information transmission, neuronal maturation and synapse formation, CNS metabolism, and damaged blood-brain barrier repair and reconstruction [48, 49]. Neurons are the basic structural and functional units of the nervous system, and the key to neural function is the synaptic signalling process, which is partly electrical and partly chemical . The essential function of neurons is to exchange messages through information input, integration, conduction and output. Thus, neurons are crucial to the sensation, learning, memory, cognition and movement of organisms [51, 52]. The apoptosis or necroptosis of microglia, astrocytes or neurons can lead to severe neural dysfunction (epilepsy, Alzheimer's disease, cerebrovascular disease, encephalitis, meningitis, etc.), or even death [53, 54]. Apoptosis and necroptosis occurred in microglia, astrocytes or neurons after A. cantonensis infection, indicating that neurotrophic agents and inhibitors of apoptosis and necroptosis could be effective in combination with anti-parasitic drugs (albendazole) and steroidal anti-inflammatory drugs (dexamethasone).
In summary, this study is the first to demonstrate that A. cantonensis infection can significantly induce the apoptosis and necroptosis of astrocytes, neurons and microglia in host brain parenchymal and hippocampal tissues. This not only enriches our understanding of A. cantonensis pathogenesis but also provides a clue to novel potential therapeutic strategies against angiostrongyliasis cantonensis.
We sincerely appreciate that Dr Zeng xin and Mr. Lin Datao provided the parasites used in the present study and we thank Mrs. Guan Yuanjun and Dr Li Xiaobo for providing help with microscopy, flow cytometry and expert technical assistance.
This work was supported by grants from the National Natural Science Foundation of China (grant nos. 81371836 and 81572023), Guangdong Natural Science Foundation (grant no. 2014A030313134), Science and Technology Planning Project of Guangdong Province (grant no. 2016A050502008), the National Key Research and Development Program of China (grant nos. 2016YFC1202003, 2016YFC1202005 and 2016YFC1200500), the Project of Basic Platform of National Science and Technology Resources of the Ministry of Sciences and Technology of China (grant no. TDRC-2017-22), Science and Technology Planning Project of Guangzhou (grant no. 201607010029), the 111 Project (grant no. B12003), the Undergraduates Innovation Training Program of Guangdong Province (grant nos. 201410558274 and 201601084) and Teaching Reform Project of Sun Yat-sen University (grant no. 2016012).
LZY and WZ conceived and designed the experiments and drafted the manuscript; ZMY participated in drafting the manuscript; ZMY, PT and XYY performed the experiments; HY, YL, HP and KO collected and analyzed the data; WYQ, PD, ZHL, DW and WZD participated in study design, technological guidance and coordination. All authors read and approved the final manuscript.
All animal procedures in this study were reviewed and approved by the Institutional Animal Care and Use Committee of Sun Yat-sen University and were operated in accordance with the regulations of the Guide for the Care and Use of Experimental Animals of the National Institutes of Health.
Lv S, Zhou XN, Andrews JR. Eosinophilic meningitis caused by Angiostrongylus cantonensis. ACS Chem Neurosci. 2017; https://doi.org/10.1021/acschemneuro.7b00233.
Kolb JP, Oguin TH 3rd, Oberst A, Martinez J. Programmed cell death and inflammation: winter is coming. Trends Immunol 2017; doi:https://doi.org/10.1016/j.it.2017.06.009.
Peña-Blanco A, García-Sáez AJ. Bax, Bak and beyond: mitochondrial performance in apoptosis. FEBS J. 2017; https://doi.org/10.1111/febs.14186.
Dossi E, Vasile F, Rouach N. Human astrocytes in the diseased brain. Brain Res Bull. 2017; https://doi.org/10.1016/j.brainresbull.2017.02.001.


text:
using namespace cpb;

void wrap_parallel(py::module& m) {
    py::class_<DeferredBase, std::shared_ptr<DeferredBase>>(m, "DeferredBase")
        .def("compute", &DeferredBase::compute)
        .def_property_readonly("solver", &DeferredBase::solver)
        .def_property_readonly("result", &DeferredBase::result);

    using DeferredXdCM = Deferred<ArrayXXdCM>;
    py::class_<DeferredXdCM, std::shared_ptr<DeferredXdCM>, DeferredBase>(m, "DeferredXd");

    m.def("parallel_for", [](py::object sequence, py::object produce, py::object retire,
                             std::size_t num_threads, std::size_t queue_size) {
        auto const size = py::len(sequence);
        py::gil_scoped_release gil_release;

        struct Job {
            py::object py;
            std::shared_ptr<DeferredBase> cpp;
        };

        parallel_for(
            size, num_threads, queue_size,
            [&produce, &sequence](size_t id) {
                py::gil_scoped_acquire gil_acquire;
                py::object var = sequence[py::cast(id)];
                py::object obj = produce(var);
                return Job{obj, obj.cast<std::shared_ptr<DeferredBase>>()};
            },
            [](Job& job) {
                // no GIL lock -> computations run in parallel
                // but no Python code may be called here
                job.cpp->compute();
            },
            [&retire](Job job, size_t id) {
                py::gil_scoped_acquire gil_acquire;
                retire(job.py, id);
                job.py.release().dec_ref();
                job.cpp.reset();
            }
        );
    }, "sequence"_a, "produce"_a, "retire"_a, "num_threads"_a, "queue_size"_a);
}

redpajama_set_name: RedPajamaGithub


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Someone asked Kate Beckinsale if her ex's girlfriend was her daughter
And her response was brilliant…
Kate Beckinsale is spending Christmas with her ex and his girlfriend
'My teenage daughter needs more strong female role models'
Helen Bownass
Kate Beckinsale talks to Stylist about her next chapter
"It's a great moment for me to become my own woman"


Can you believe Christmas is almost here again?! To celebrate that fact, as well as the overwhelcoming response to "Little Drummer Boy" last year, for KING & COUNTRY has prepared a bit of a gift... they went back into the studio and recorded a "Rewrapped" drum-filled version of the song.
And with it, they wanted to give you a rewrapped visual depiction as well! So here's "Little Drummer Boy (REWRAPPED)" the song, and LIVE music video - featuring footage from last year's tour.
Check out all the dates on their upcoming Christmas tour "Little Drummer Boy - The Christmas Tour," as well as the ones coming to Charlotte, NC and Raleigh, NC!


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Q: Youtube Api rate (like-dislike) post request not working I want to post rate with Youtube Data Api. I posted this link with curl : https://www.googleapis.com/youtube/v3/videos/rate?access_token=xxxxTOKENxxxxx&id=xxxxVIDEO_IDxxxxx&rating=dislike&key=xxxxAPI_KEYxxxxx
This request was returning 204 HTTP Code. But when I checked video, rate statistics not change. Where am i doing wrong ?
I wrote rate post request with Google PHP Library. These are my codes;
session_start();
require_once 'vendor/autoload.php';

$client = new Google_Client();
$client->setAuthConfig('client.json');
$scope = "https://www.googleapis.com/auth/youtube https://www.googleapis.com/auth/youtube.force-ssl https://www.googleapis.com/auth/youtube.readonly https://www.googleapis.com/auth/youtube.upload https://www.googleapis.com/auth/youtubepartner https://www.googleapis.com/auth/youtubepartner-channel-audit";
$client->addScope($scope);
$client->setRedirectUri('http://localhost/youtube/islem.php');

if (isset($_GET['code'])) {
    $client->authenticate($_GET['code']);

    $access_token = $client->getAccessToken();
    $_SESSION['access_token'] = $client->getAccessToken();
    header("Location: islem.php");
} else {
    $client->setAccessToken($_SESSION['access_token']);
}

$videoID = "xxxxxxxxx";
$youtube = new Google_Service_YouTube($client);
$result = $youtube->videos->rate($videoID, "like");

print_r($result);

A: This is working for me. I tried the Videos.rate Try-It and filled in the necessary details and it worked. I was able to like a random video on Youtube by obtaining the videoId. I used the Try-it to remove the like (thumbs up) and it still works accordingly.
Try using the URI request in the Try-It generated when you press the EXECUTE button. Make sure you're logged-in to Youtube as well.

redpajama_set_name: RedPajamaStackExchange


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Rent-A-Center Announces Nationwide Rollout of eCommerce Solution
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Online Shopping Convenience Reaches New and Return Customers
PLANO, Texas--(BUSINESS WIRE)--Dec. 6, 2016-- Rent-A-Center, Inc. (NASDAQ/NGS:RCII), the nation's largest rent-to-own operator, announced that their nationwide rollout of an end-to-end eCommerce solution is substantially complete. Customers now have the ability to fully transact with Rent-A-Center online from the convenience of their desktop, laptop, or mobile device.
"eCommerce is attracting customers who appreciate the new option to shop and complete sales transactions online and then have products delivered to their homes," says Robert Davis, CEO. "In fact, more than 70 percent of our online customers are shoppers who are either new to Rent-A-Center or who have not done business with us in over one year."
Rent-A-Center currently offers more than 73 products available to rent online, primarily consumer electronics.
"So far, we've seen demand for the latest Sony and Microsoft gaming systems, Sony, LG and VIZIO TVs, Samsung smartphones, as well as laptops from ASUS and Toshiba," says Angela Yochem, CIO and Senior Vice President – Information Technology. "Enabling digital business is key to our strategy as we continue to expand our product offerings and enhance our customer interactions. Since our customers engage with us across all channels, this type of innovation expands our ability to serve our customers, deepen those relationships, and to reach new customers in the ever-evolving market."
Included as part of Rent-A-Center's eCommerce solution, shoppers browsing rentacenter.com's website now also have the option to complete an online form and obtain preapproval to rent from within one of Rent-A-Center's approximately 2,600 store locations.
"Once approved, customers coming into our stores enjoy a more efficient and streamlined in-store shopping experience since their preapproval information is already loaded into our systems," says Yochem. "Our customers tell us they appreciate the convenience of being able to obtain pre-approval online."
Rent-A-Center's eCommerce solution brings the benefits of rent-to-own to consumers, regardless of where they choose to shop. For a new and returning market of consumers, that means access to the quality products they want and need for their homes is now just "a click away."
About Rent-A-Center, Inc.
A rent-to-own industry leader, Plano, TX-based, Rent-A-Center, Inc., is focused on improving the quality of life for its customers by providing them the opportunity to obtain ownership of high-quality, durable products such as consumer electronics, appliances, computers, furniture and accessories, and smartphones, under flexible rental purchase agreements with no long-term obligation. The Company owns and operates approximately 2,600 stores in the United States, Mexico, Canada and Puerto Rico, and approximately 1,870 Acceptance Now locations in the United States and Puerto Rico. Rent-A-Center Franchising International, Inc., a wholly owned subsidiary of the Company, is a national franchiser of approximately 230 rent-to-own stores operating under the trade names of "Rent-A-Center," "ColorTyme," and "RimTyme." For additional information about the Company, please visit our website at www.rentacenter.com.
This press release contains forward-looking statements that involve risks and uncertainties. Such forward-looking statements generally can be identified by the use of forward-looking terminology such as "may," "will," "expect," "intend," "could," "estimate," "should," "anticipate," or "believe," or the negative thereof or variations thereon or similar terminology. The Company believes that the expectations reflected in such forward-looking statements are accurate. However, there can be no assurance that such expectations will occur. The Company's actual future performance could differ materially from such statements. Factors that could cause or contribute to such differences include, but are not limited to: the Company's ability to develop and successfully execute strategic initiatives; the Company's ability to successfully implement its new store information management system; the Company's ability to develop and successfully implement virtual or e-commerce capabilities; the Company's ability to identify and successfully market products and services that appeal to its customer demographic; consumer preferences and perceptions of the Company's brand; the Company's ability to enter into new and collect on its rental or lease purchase agreements; the Company's compliance with applicable statutes or regulations governing its transactions; information technology and data security costs; the impact of any breaches in data security or other disturbances to the Company's information technology and other networks and the Company's ability to protect the integrity and security of individually identifiable data of its customers and employees; and the other risks detailed from time to time in the Company's SEC reports, including but not limited to, its Annual Report on Form 10-K for the year ended December 31, 2015, and its Quarterly Reports on Form 10-Q for the quarters ended March 31, 2016, June 30, 2016, and September 30, 2016. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this press release. Except as required by law, the Company is not obligated to publicly release any revisions to these forward-looking statements to reflect the events or circumstances after the date of this press release or to reflect the occurrence of unanticipated events.
Source: Rent-A-Center, Inc.
Rent-A-Center, Inc.
Maureen Short, 972-801-1899
maureen.short@rentacenter.com
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The Young & the Reckless 'The Young & the Reckless' (EP stream)
Vancouver indie rocker Greg Pothier currently leads the multi-membered garage troupe Dirty Spells, but also moonlights in the studio with another enormous pop crew called the Young & Reckless. This time around, Pothier's focusing on the softened sounds of '60s pop, as evidenced by the troupe's three-song, self-titled EP.
The mini-effort was tracked at Chains of Love/Vancouver studio guru Felix Fung's Little Red Sounds, and likewise features guest musicians from that retro-flavoured act, as well as the Ballantynes, the Radii, Dirty Spells, Pleasure Cruise, Fine Times and more. The songs favour lilting string arrangements, gently go-going rhythms and hushed female vocals, and fit somewhere between Belle and Sebastian's twee-soul and a batch of uncovered Lulu recordings. You can check out the EP down below.
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