text:
\section{Introduction}

Lagrangian formulation of interacting higher spin field theory is a
fundamental unsolved problem of classical field theory during long
time (see e.g. the reviews \cite{reviews}). The essence of the
problem is that any naive (e.g. minimal) including the interaction
to free higher spin field Lagrangian violates consistency of the
equations of motion (see the various aspects of the inconsistency in
\cite{consist,consist1,consist2}). One of the partial aspects of the
generic problem is a Lagrangian formulation for higher spin fields
coupled to external background. At present, all known consistent
Lagrangian formulations are constructed only on space of constant
curvature without any other external fields. Then a natural question
arises if there exist the other background fields admitting the
consistent Lagrangian formulation for higher spin fields. For
example, if to accept that the massive higher spin fields have the
superstring origin, the evident background in bosonic sector is
formed by the fields from massless string spectrum what corresponds
in sigma-model approach \cite{FT} to manifold endowed with Riemann
metric and additional external scalar (dilaton), vector and totally
antisymmetric third rank tensor field which can be associated with
torsion. In principle one can hope that the consistent Lagrangian
formulation of higher spin fields coupled to background fields
actually exists under some equations linking all the background
fields.

In this note we consider the free massive higher spin bosonic field
theory coupled to external metric, vector field and arbitrary third
rank tensor field and assume that the Lagrangian contains no inverse
mass terms. At these conditions we prove that the only manifold
admitting the consistent Lagrangian formulation is constant
curvature space with vanishing scalar, vector and third rank tensor
external fields. The proof is based on generic BRST formulation of
higher spin field theory (see the various use of BRST formalism in
higher spin field theory in
\cite{BRSThsf,0611,bkl,brst1,BRSThsf1,mg}
which allows efficiently
to study the bosonic and fermionic, massless and massive higher spin
fields, to take into account a gauge structure of the theory and to
work with tensor fields of various symmetry of indices.

The BRST approach to Lagrangian construction for higher spin fields,
which is developed in our papers, is realized as follows. The
mass-shell equation and subsidiary conditions are treated as a part
of the first class constraints of some unknown yet gauge theory. The
new constraints are added to initial ones to form a complete set of
first class constraints. All the constraints are formulated as the
operators acting in auxiliary Fock space and it is assumed that the
algebra of the constraints in terms of commutators is closed. Taking
into account these constraints one can construct the Hermitian
nilpotent BRST-BFV operator $Q$ \cite{BF} and find higher spin field
Lagrangian in terms of the $Q$. Nilpotency of the $Q$ guarantees a
gauge invariance of the corresponding action. As a result we get the
higher spin field Lagrangian which automatically contains all the
auxiliary fields. Such an approach has been completely realized in
$d$-dimensional flat and AdS spaces and its different aspects have
been studied in \cite{BRSThsf,0611,bkl,BRSThsf1}. The essential
basic element of such approach was closure of the algebra of
operator constraints.

To realize this approach for the fields on some background
first of all we should find the corresponding mass-shell and subsidiary
conditions. For bosonic fields in flat space they are Klein-Gordon
equation and the conditions for the fields to be divergence free and
traceless (see e.g. \cite{bk})
\begin{eqnarray}
(\partial^2-m^2)\varphi_{\mu_1\ldots\mu_s}=0,
\qquad
\partial^{\mu_1}\varphi_{\mu_1\ldots\mu_s}=0,
\qquad
\eta^{\mu_1\mu_2}\varphi_{\mu_1\mu_2\ldots\mu_s}=0.
\label{EM-flat}
\end{eqnarray}
In case of fields on a background all the conditions (\ref{EM-flat})
should be deformed by the proper way. For the bosonic fields in AdS
space such deformations has been constructed in \cite{bkl}. It is
interesting to point out that in the case of fields in AdS space the
corresponding closed algebra of constraints belongs to class of
quadratic non-linear algebra and finding the nilpotent BRST operator
is a very nontrivial problem (see e.g. \cite{NvH}). In the case
under consideration we should construct a deformation of the
constraints (\ref{EM-flat}), realizing all the conditions as the
operator constraints and find the restrictions on the background
when their algebra will be closed.

We assume that a manifold under consideration is endowed with metric
$g_{\mu\nu}$, the background vector $A_{\mu}$ and third rank tensor
$K_{\mu\nu\alpha}$ field with no index symmetry, so that the torsion
tensor is a particular case of $K_{\mu\nu\alpha}$ tensor.
The covariant derivatives are constructed with the use of
Christoffel symbols $
\Gamma^\alpha_{\mu\nu}=\frac{1}{2}g^{\alpha\beta} (\partial_\mu
g_{\beta\nu}+\partial_\nu g_{\mu\beta}-\partial_\beta g_{\mu\nu}). $

Introduce the auxiliary Fock space generated by bosonic creation and
annihilation operators with tangent space indices
($a,b=0,1,\ldots,d-1$)
\begin{eqnarray}
[a_a,a^+_b]=\eta_{ab},
\qquad
\eta_{ab}=diag(-,+,\ldots,+).
\label{a-bos}
\end{eqnarray}
An arbitrary vector in this Fock space has the form
\begin{eqnarray}
\label{PhysState}
|\varphi\rangle
&=&
\sum_{s=0}^{\infty}\varphi_{a_1\ldots\,a_s}(x)\,
a^{+a_1}\ldots\,a^{+a_s}|0\rangle
=
\sum_{s=0}^{\infty}\varphi_{\mu_1\ldots\,\mu_s}(x)\,
a^{+\mu_1}\ldots\,a^{+\mu_s}|0\rangle
\equiv
\sum_{s=0}^{\infty}|\varphi_s\rangle
,
\end{eqnarray}
where
$a^{+\mu}(x)=e^\mu_a(x)a^{+a}$, $a^\mu(x)=e^\mu_a(x)a^a$,
with $e^\mu_a(x)$ being the vielbein.
It is evident that $[a_\mu, a_\nu^+]=g_{\mu\nu}$.
We also
suppose the standard relation
$\nabla_\mu e^a_\nu=\partial_\mu e^a_\nu-\Gamma^\alpha{}_{\nu\mu}e^a_\alpha
+\omega_\mu{}^a{}_be^b_\nu=0$, where $\omega_\mu{}^a{}_b$ is the spin connection.

Then one
introduces derivative operator
\begin{eqnarray}
D_\mu=\partial_\mu+\omega_\mu^{ab}a_a^+a_b, &\qquad& D_\mu|0\rangle=0
\label{D_mu}
\end{eqnarray}
which acts on states of the Fock space (\ref{PhysState}) as the covariant
derivative
\begin{eqnarray}
D_\mu|\varphi_s\rangle=(\nabla_\mu\varphi_{\mu_1\ldots\,\mu_s})\,
a^{+\mu_1}\ldots\,a^{+\mu_s}|0\rangle
\end{eqnarray}
and tries to realize the generalization of equations (\ref{EM-flat}) in the operator
form
\begin{eqnarray}
l_0|\varphi_s\rangle=
l_1|\varphi_s\rangle=
l_2|\varphi_s\rangle=
0
\label{EM-op}
\end{eqnarray}
where operators $l_0$, $l_1$, $l_2$ corresponding to Klein-Gordon,
divergence free and traceless equations respectively.

The procedure of Lagrangian construction based on the BRST method looks as follows.
For the Lagrangian be a real function the BRST operator used for its construction must
be a Hermitian operator. It assumes that the set of operators underlying the BRST
operator must be invariant under Hermitian conjugation.
To have such a set of operators we add to constraints $l_0$, $l_1$, $l_2$ their
Hermitian conjugated operators $l_1^+$, $l_2^+$
with $l_0$ being assumed to be self-conjugated.
Then for constructing the BRST operator the underlying set of
operators must form an algebra.
To get the algebra we must add to operators $l_0$, $l_1$, $l_2$, $l_1^+$, $l_2^+$ some more operators providing closing the algebra.
But if we want to construct with the help of the obtained algebra
Lagrangian for spin-s field, then this algebra must be a deformation
of the algebra in Minkowski or in AdS \cite{bkl}
space. Thus we can add only two operators which are generalization
of operators
\begin{eqnarray}
g_0=a_\mu^+a^\mu+\tfrac{d}{2},
\qquad
g_m=m^2+const
\label{g0}
\end{eqnarray}
to the case of curved space. Since operator $g_0$ is dimensionless
and we do not consider terms with inverse powers of the mass then it
is impossible to deform operator $g_0$ by terms with the curvature or with
the background fields.\footnote{We adopt that the backgound fields
have mass dimension one like the torsion.}
Therefore operator $g_0$ keeps the same form (\ref{g0}) as in the
flat case. As for possible generalization of operator $g_m$ we postpone this question.
Thus we came to the conclusion that
in
order to be possible to construct Lagrangian with the help of the BRST method
we must find explicit expressions for the operators
\begin{eqnarray}
l_0,\qquad l_1,\qquad l_1^+,\qquad l_2,\qquad l_2^+,\qquad g_0,\qquad g_m
\label{set-R}
\end{eqnarray}
so that they form an algebra.\footnote{\label{fnote}It should be note that in general case, operators $l_0$, $l_1$, $l_2$
may not coincide with that given in (\ref{EM-op}).
We demand here only that operators (\ref{set-R}) have the proper free limit.
The consistent conditions on the field (\ref{EM-op}) will be followed from the BRST construction.}
If we find algebra different from the AdS case,
then it means that there is a hope to construct Lagrangian in space
different from AdS.

We will deform the operators by introducing background fields.
We explore the case when the background fields are vector and third rank
tensor with dimension of mass.
Note that any third rank tensor can be decomposed into totally
symmetric $S_{(\mu\nu\sigma)}$, totally antisymmetric $A_{[\mu\nu\sigma]}$
tensors, and tensors with mixed symmetry of the indices (see e.g.
\cite{0611263}).
We consider the case of the decomposition when the mixed symmetry tensors
have the following symmetry of the indices
\begin{eqnarray}
\label{M-sym}
M_{\mu\nu\sigma}=-M_{[\nu\mu]\sigma}\,,
&&
M_{[\mu\nu\sigma]}=0\,.
\end{eqnarray}
In addition we adopt that all the background tensors are traceless,
absorbing their traces into vector field $V_\mu$.

Let us discuss possible form of the operators.
First, the dimensionless operators
\begin{eqnarray}
 \label{l2}
l_2={\textstyle\frac{1}{2}}\,a^\mu a_\mu
\,,
\qquad
l_2^+=\tfrac{1}{2}a^+_\mu a^{\mu+}
\,,
\qquad
g_0=a_\mu^+a^\mu+\tfrac{d}{2}
\end{eqnarray}
can't be modified by the background fields if we don't take into account the mass in the inverse powers.

Next let us consider operator $l_1$ responsible for the physical
field to be divergence free. Since this operator has mass dimension
one then the background fields are introduced linearly in $l_1$.
Also we note that in the terms with the background fields the
creation and annihilation operators, if they not contracted with the
background fields, are contracted with each other and these
contractions can be expressed through the operators $l_2$, $l_2^+$,
$g_0$ (\ref{l2}). Therefore the most general expression for the
operator $l_1$ is
\begin{eqnarray}
l_1&=&a^\mu D_\mu
+\sum_{k,m=0}^{\infty}\alpha_{km}\; V_\mu a^\mu\;(l_2^+)^m \; g_0^k  \; l_2^m
+\sum_{k,m=0}^{\infty}\omega_{km}\; V_\mu a^{+\mu}\;(l_2^+)^m \; g_0^k \; l_2^{m+1}
\nonumber
\\
&&{}+\sum_{k,m=0}^{\infty}\beta_{km}\; M_{[\mu\nu]\sigma} a^{+\mu}a^\nu a^\sigma\;
(l_2^+)^m \; g_0^k \; l_2^m
+\sum_{k,m=0}^{\infty}\sigma_{km}\; M_{[\mu\nu]\sigma}
a^{+\nu}a^{+\sigma}a^\mu\;(l_2^+)^m \; g_0^k  \; l_2^{m+1}
\nonumber
\\
&&{}+\sum_{k,m=0}^{\infty}\epsilon_{km}\;S_{(\mu\nu\sigma)}a^{+\mu} a^{+\nu} a^{+\sigma}
\;(l_2^+)^m \; g_0^k \; l_2^{m+2}
+\sum_{k,m=0}^{\infty}\zeta_{km}\;S_{(\mu\nu\sigma)}a^{+\mu} a^{+\nu}a^{\sigma}
\;(l_2^+)^m \; g_0^k  \; l_2^{m+1}
\nonumber
\\
&&{}+\sum_{k,m=0}^{\infty}\gamma_{km}\;S_{(\mu\nu\sigma)}a^{+\mu}a^{\nu}a^{\sigma}
\;(l_2^+)^m \; g_0^k \; l_2^m
+\sum_{k,m=0}^{\infty}\theta_{km}\;S_{(\mu\nu\sigma)}a^{\mu}a^{\nu}a^{\sigma}
\;(l_2^+)^{m+1} \; g_0^k \; l_2^m
\label{l1}
\end{eqnarray}
with arbitrary coefficients
$\alpha_{km}$, $\beta_{km}$, $\gamma_{km}$, $\omega_{km}$,
$\sigma_{km}$, $\epsilon_{km}$, $\zeta_{km}$, $\theta_{km}$.
The totally antisymmetric tensor $A_{[\mu\nu\sigma]}$ cannot be introduced
into $l_1$ since any its contraction with creation and annihilation operators
gives zero. But it should be noted that in case we considered the dynamics of a field
with mixed symmetry of the indices in the background fields then the totally
antisymmetric field $A_{[\mu\nu\sigma]}$ could be introduced into $l_1$.

Taking Hermitian conjugation (\ref{l1}) and moving operators
$l_2^+$, $g_0$, $l_2$
to the right we obtain expression for the operator $l_1^+$
\begin{eqnarray}
l_1^+
&=&
-a^{+\mu} D_\mu
+\sum_{k,m=0}^{\infty}\alpha'_{km}\;V_\mu a^{+\mu}\;(l_2^+)^m \; g_0^k\;l_2^m
+\sum_{k,m=0}^{\infty}\omega'_{km}\;V_\mu a^\mu \;(l_2^+)^{m+1}\;g_0^k\;l_2^m
\nonumber
\\
&&{}+\sum_{k,m=0}^{\infty}\beta'_{km}\;M_{[\mu\nu]\sigma}a^{+\nu}a^{+\sigma}a^\mu
\;(l_2^+)^m \; g_0^k \; l_2^m
+\sum_{k,m=0}^{\infty}\sigma'_{km}\;M_{[\mu\nu]\sigma}a^{+\mu}a^\nu a^\sigma
\;(l_2^+)^{m+1} \; g_0^k \; l_2^m
\nonumber
\\
&&{}
+\sum_{k,m=0}^{\infty}\epsilon'_{km}\;S_{(\mu\nu\sigma)}a^\mu a^\nu a^\sigma
\;(l_2^+)^{m+2} \; g_0^k \; l_2^m
+\sum_{k,m=0}^{\infty}\zeta'_{km}\;S_{(\mu\nu\sigma)}a^{+\mu}a^\nu a^\sigma
\;(l_2^+)^{m+1} \; g_0^k \; l_2^m
\nonumber
\\
&&{}
+\sum_{k,m=0}^{\infty}\gamma'_{km}\;S_{(\mu\nu\sigma)}a^{+\mu}a^{+\nu}a^{\sigma}
\;(l_2^+)^m \; g_0^k \; l_2^m
\nonumber
\\
&&{}
+\sum_{k,m=0}^{\infty}\theta'_{km}\;S_{(\mu\nu\sigma)}a^{+\mu}a^{+\nu}a^{+\sigma}
\;(l_2^+)^m \; g_0^k \; l_2^{m+1}
\label{l1+}
\end{eqnarray}
where the primed coefficients can be expressed through non-primed
ones and vice versa.
Moreover the dependent and independent coefficients can be chosen in a variety
of ways, choosing as independent coefficients partially both primed and non-primed coefficients.
Note that the terms containing at least one of
the operators $l_2^+$, $g_0$, $l_2$ don't influence on closing the
algebra (and as a consequence on the background geometry) and this
fact we denote as follows
\begin{eqnarray}
l_1&\approx&a^\mu D_\mu
+\alpha_{00}\; V_\mu a^\mu
+\beta_{00}\; M_{[\mu\nu]\sigma} a^{+\mu}a^\nu a^\sigma
+\gamma_{00}\;S_{(\mu\nu\sigma)}a^{+\mu}a^{\nu}a^{\sigma}
\label{l1a}
\\
l_1^+
&\approx&
-a^{+\mu} D_\mu
+\alpha'_{00}\;V_\mu a^{+\mu}
+\beta'_{00}\;M_{[\mu\nu]\sigma}a^{+\nu}a^{+\sigma}a^\mu
+\gamma'_{00}\;S_{(\mu\nu\sigma)}a^{+\mu}a^{+\nu}a^{\sigma}
\label{l1+a}
\end{eqnarray}
where $\approx$ means ``up to terms proportional to operators $l_2^+$, $g_0$, $l_2$''.
Also we note that $\alpha_{00}$, $\alpha_{00}'$, $\beta_{00}$,
$\beta_{00}'$, $\gamma_{00}$, $\gamma'_{00}$ can be considered as
independent of each other.

Let us consider commutators
\begin{eqnarray}
[\,l_1,l_2]\approx\gamma_{00}\; S_{(\mu\nu\sigma)}a^{\mu} a^{\nu} a^{\sigma}
\,,
&\qquad&
[\,l_1^+,l_2^+]\approx\gamma'_{00}\; S_{(\mu\nu\sigma)}a^{+\mu} a^{+\nu} a^{+\sigma}
\,.
\end{eqnarray}
We see that to close the algebra we must demand $\gamma_{00}=\gamma'_{00}=0$.
This means that the totally symmetric tensor $S_{(\mu\nu\sigma)}$ cannot
influence on the background geometry.

Next we consider commutators
\begin{eqnarray}
[\,l_1,l_2^+] &\approx& a^{+\mu}D_\mu+\alpha_{00}\; V_\mu a^{+\mu}
-\beta_{00} \; M_{[\mu\nu]\sigma} a^{+\nu}a^{+\sigma}a^\mu
\nonumber
\\
&\approx&-l_1^++(\alpha_{00}+\alpha'_{00})\; V_\mu a^{+\mu}
+(\beta'_{00}-\beta_{00}) \; M_{[\mu\nu]\sigma} a^{+\nu}a^{+\sigma}a^\mu
\,,
\\
{}
[l_1^+,l_2]&\approx&
l_1-(\alpha_{00}+\alpha'_{00})\; V_\mu a^{\mu}
+(\beta'_{00}-\beta_{00}) \; M_{[\mu\nu]\sigma}a^{+\mu}a^{\nu}a^{\sigma}
\,,
\end{eqnarray}
and for their closing it is necessary to put $\alpha'_{00}=-\alpha_{00}$
and $\beta'_{00}=\beta_{00}$.
Thus operators $l_1$ and $l_1^+$
will take the form
\begin{eqnarray}
l_1&\approx&a^\mu D_\mu+\alpha_{00}V_\mu a^\mu+\beta_{00}M_{[\mu\nu]\sigma} a^{+\mu}a^\nu a^\sigma
\label{l1b}
\\
l_1^+
&\approx&
-a^{+\mu} D_\mu-\alpha_{00}V_\mu a^{+\mu}+\beta_{00}M_{[\mu\nu]\sigma}a^{+\nu}a^{+\sigma}a^\mu
\label{l1+b}
\end{eqnarray}

Let us now consider commutator
\begin{eqnarray}
[l_1^+,l_1]&\sim&
D^2
+P^{\mu\alpha\sigma}a^+_\mu a_\alpha D_\sigma
+2\alpha_{00}V^\sigma D_\sigma
+W^{\mu\nu\alpha\beta}a^+_\mu a^+_\nu a_\alpha a_\beta
+K^{\mu\alpha}a^+_\mu a_\alpha
+Z
\,,
\label{l1+l1}
\end{eqnarray}
where
\begin{eqnarray}
&&
D^2=g^{\mu\nu}(D_\mu D_\nu-\Gamma^\sigma{}_{\mu\nu}D_\sigma)\,,
\\
&&
\label{P}
P^{\mu\alpha\sigma}=2\beta_{00}(M^{\mu(\alpha\sigma)}-M^{\alpha(\mu\sigma)})
=-P^{\alpha\mu\sigma}\,,
\\
&&
W_{\mu\nu\alpha\beta}=R_{\mu\alpha\beta\nu}
-\beta_{00}\bigl[\nabla_{(\beta} M_{\alpha)\mu\nu}+\nabla_{(\mu} M_{\nu)\alpha\beta}\bigr]
\nonumber
\\
&&
\mspace{82mu}{}
+\beta_{00}^2\bigl[M_{\tau(\mu\nu)}M^\tau{}_{(\alpha\beta)}
-4M_{\alpha(\tau\mu)}M_{\nu(\beta}{}^{\tau)}\bigr]
\,,
\\
&&
K_{\mu\alpha}=R_{\mu\alpha}
-2\beta_{00}\nabla^\sigma M_{\alpha(\mu\sigma)}
-2\beta_{00}^2M_{\mu(\rho\tau)}M_\alpha{}^{\rho\tau}
\nonumber
\\
&&
\mspace{82mu}{}
+\alpha_{00}(\nabla_\alpha V_\mu-\nabla_\mu V_\alpha)
+2\alpha_{00}\beta_{00}(M_{\mu(\alpha\sigma)}-M_{\alpha(\mu\sigma)})V^\sigma
\,,
\\
&&
Z=\alpha_{00}^2V_\mu V^\mu+\alpha_{00}\nabla_\mu V^\mu
\end{eqnarray}
and $\sim$ means ``up to terms proportional to operators
$l_1$, $l_1^+$, $l_2$, $l_2^+$, $g_0$''.
In order to have a closed algebra we have to suppose that the right hand side
of (\ref{l1+l1}) be proportional to operators of the algebra (\ref{set-R}).
For example we may define operators $l_0$ and $g_m$ as follows
\begin{eqnarray}
&&
l_0\sim
D^2-m^2
+P^{\mu\alpha\sigma}a^+_\mu a_\alpha D_\sigma
+2\alpha_{00}V^\sigma D_\sigma
+W^{\mu\nu\alpha\beta}a^+_\mu a^+_\nu a_\alpha a_\beta
+K^{\mu\alpha}a^+_\mu a_\alpha
+Z
\,,
\label{l0}
\\
&&
g_m=m^2
\,.
\end{eqnarray}

Let us turn to the commutator $[l_1^+,l_0]$ and consider terms with two
derivative operators. One has
\begin{eqnarray}
[l_1^+,l_0]&\sim&P^{\alpha(\mu\sigma)}a_\alpha^+ D_{(\mu}D_{\sigma)}+\ldots
\end{eqnarray}
Demanding that this commutator
be proportional to operators (\ref{set-R})
and since we are working with traceless fields, then  one has to suppose
\begin{eqnarray}
P^{\alpha(\mu\sigma)}=0.
\end{eqnarray}
If $\beta_{00}\neq0$, then taking into account first (\ref{P}) and then (\ref{M-sym}) we come to the
conclusion that $M_{\mu\nu\sigma}=M_{[\mu\nu\sigma]}=0$.
To avoid $M_{\mu\nu\sigma}=0$ we will adopt less strong condition that $\beta_{00}=0$.
In any case
this means that the background field $M_{[\mu\nu]\sigma}$ cannot influence
on the background geometry.

Now commutator $[l_1^+,l_0]$ takes the form
\begin{eqnarray}
[l_1^+,l_0]&\sim&
4a^{+\mu}a^{+\nu}a^\alpha R^\sigma{}_{\mu\nu\alpha}D_\sigma
+(2R^{\mu\sigma}+3\alpha_{00}F^{\sigma\mu})a_\mu^+ D_\sigma
-R_{\mu\alpha\beta\nu;\sigma}a^{\mu+}a^{\nu+}a^{\sigma+}a^\alpha a^\beta
\nonumber
\\
&&{}
+(4\alpha_{00}R^\sigma{}_{\mu\nu\alpha}V_\sigma-R_{\mu\nu;\alpha}
+\alpha_{00}\nabla_\mu F_{\nu\alpha})a^{+\mu}a^{\nu+}a^\alpha
\nonumber
\\
&&{}
+a^{+\mu}\alpha_{00}
\Bigl[
3\alpha_{00}F_{\sigma\mu}V^\sigma
+\nabla^\nu F_{\nu\mu}
+2V^\sigma R_{\sigma\mu}
\Bigr]
\,,
\label{l1+l0}
\end{eqnarray}
where $F_{\mu\nu}=\nabla_\mu V_\nu-\nabla_\nu V_\mu$.
We see that commutator (\ref{l1+l0}) does not proportional to the
operators (\ref{set-R}) if the curvature and the background vector field $V_\mu$
are arbitrary.
To find conditions on the curvature and $V_\mu$ which are necessary
for closing the algebra
we decompose the Riemann tensor into irreducible parts
\begin{eqnarray}
R_{\mu\nu\alpha\beta}&=&
C_{\mu\nu\alpha\beta}
+\frac{1}{d-2}\left(
\tilde{R}_{\mu\alpha}g_{\nu\beta}+\tilde{R}_{\nu\beta}g_{\mu\alpha}
-\tilde{R}_{\mu\beta}g_{\nu\alpha}-\tilde{R}_{\nu\alpha}g_{\mu\beta}
\right)
\nonumber
\\
&&{}
+\frac{R}{d(d-1)}(g_{\mu\alpha}g_{\nu\beta}-g_{\mu\beta}g_{\nu\alpha}),
\end{eqnarray}
where $C_{\mu\nu\alpha\beta}$ is the Weyl tensor,
$\tilde{R}_{\mu\nu}=R_{\mu\nu}-\frac{1}{d}g_{\mu\nu}R$ is the traceless part
of the Ricci tensor, and substitute this decomposition into (\ref{l1+l0})
\begin{eqnarray}
[l_1^+,l_0]&\sim&
4a^{+\mu}a^{+\nu}a^\alpha C^\sigma{}_{\mu\nu\alpha}D_\sigma
+3\alpha_{00}F^{\sigma\mu}a_\mu^+ D_\sigma
-C_{\mu\alpha\beta\nu;\sigma}a^{\mu+}a^{\nu+}a^{\sigma+}a^\alpha a^\beta
\nonumber
\\
&&{}
+\Bigl[\alpha_{00}4C^\sigma{}_{\mu\nu\alpha}V_\sigma
+\tilde{R}_{\mu\alpha;\nu}-\tilde{R}_{\mu\nu;\alpha}
+\alpha_{00}\nabla_\mu F_{\nu\alpha}
\Bigr]a^{+\mu}a^{\nu+}a^\alpha
\nonumber
\\
&&{}
+a^{+\mu}
\Bigl[
3\alpha_{00}^2F_{\sigma\mu}V^\sigma
+\alpha_{00}\nabla^\sigma F_{\sigma\mu}
-\frac{(d-2)(d-4)}{4d(d-1)}\nabla_\mu R
\Bigr]
.
\label{l1+l0-}
\end{eqnarray}
From first term of r.h.s. of (\ref{l1+l0-}) we find that it is necessary to suppose
\begin{eqnarray}
C_{\mu(\alpha\beta)\nu}=0\,,
&\qquad&
\alpha_{00}F_{\mu\nu}=\alpha_{00}(\nabla_\mu V_\nu-\nabla_\nu V_\mu)=0\,.
\label{cond1}
\end{eqnarray}
The left condition in (\ref{cond1}) together with the index symmetry
of the Weyl tensor tells us that the Weyl tensor is completely
antisymmetric $C_{\mu\alpha\beta\nu}=C_{[\mu\alpha\beta\nu]}$, and
due to the Bianchi identity $C_{\mu[\alpha\beta\nu]}=0$ it equals to
zero. To satisfy the right condition in (\ref{cond1}) we can put
$\alpha_{00}=0$ or $F_{\mu\nu}=0$, after that field $V_\mu$
disappears in the r.h.s. (\ref{l1+l0-}). In particular, if the
coefficient $\alpha_{00}$ is somehow fixed, e.g. the vector field
enters the constraints through the $U(1)$ covariant derivative, ones
get immediately that $F_{\mu\nu}=0$. This means in general that
under the above assumptions the vector field $V_\mu$ does not
influence on closing the algebra and as a consequence on the
background geometry.

Next, from the second line of (\ref{l1+l0-}) we find
\begin{eqnarray}
\tilde{R}_{\alpha(\mu;\nu)}=\tilde{R}_{\mu\nu;\alpha}
\label{cond2}
\end{eqnarray}
where we have used (\ref{cond1}).
Contracting indices $\mu$ and $\nu$ in (\ref{cond2}) and using the Bianchi
identity one gets
\begin{eqnarray}
\nabla_\mu R=0
&\Rightarrow&
R=const.
\label{cond2+}
\end{eqnarray}
As a result, the background geometry must be a constant curvature
space-time.

Thus we have shown that in the higher spin field theory the
background vector and third rank tensor cannot have influence on the
geometry of the space which must be only a constant curvature one.

Let us consider the case when the background fields are introduced
into the operators being multiplied on some operators of the
algebra, like, for example, they are introduced in the operator
$l_1$ (\ref{l1}), except the terms with coefficients $\alpha_{00}$,
$\beta_{00}$, $\gamma_{00}$. In this case we expect that the
background fields will make no effects, at least on the physical
field, the same as in quantization of gauge theories a redefinition
of constraints by terms proportional to constraints have no effect
on the physical states. In case of higher spin theory we illustrate
this on a simplified example.

Let the operators have the following form
\begin{align}
\label{EM-l0}
&l_0=\partial^2-m^2+\alpha_1 g_0+\alpha_2 g_0^2
\\
& l_1=a^\alpha \partial_\alpha && l_1^+=-a^{+\mu}\partial_\mu && g_m=m^2
\\
& l_2=\tfrac{1}{2}a_\mu a^\mu && l_2^+=\tfrac{1}{2}a_\mu^+ a^{+\mu}
&&g_0=a_\mu^+ a^\mu+\tfrac{d}{2}
\label{EM-g0}
\end{align}
where $\alpha_1$  and $\alpha_2$ are some combinations of the
background fields with the dimension of mass squared. Since
$\alpha_1$ and $\alpha_2$ are multiplied on operator of the algebra,
then the algebra is closed at any $\alpha_1$ and $\alpha_2$. To
simplify the subsequent calculations we adopt $\alpha_1$ and
$\alpha_2$ are constants. At first glance it seems that the mass
shell equation which we will reproduce using the BRST method must
will be $l_0|\Phi\rangle=0$, but as we shall show it will turn out
to be $(\partial^2-m^2)|\Phi\rangle=0$, thus removing all the
dependence on $\alpha$'s (this is what we mean in
footnote~\ref{fnote} at page~\pageref{fnote}). In case of constant
$\alpha$'s the algebra of operators (\ref{EM-l0})--(\ref{EM-g0}) has
the following non-vanishing commutators
\begin{align}
&[l_1^+,l_1]=l_0+g_m-\alpha_1g_0-\alpha_2g_0^2,
\\
&[l_0,l_1]=-2\alpha_2g_0l_1-(\alpha_1+\alpha_2)l_1,
&&[l_2^+,l_1]=l_1^+,
\\
&[l_0,l_1^+]=2\alpha_2l_1^+g_0+(\alpha_1+\alpha_2)l_1^+,
&&[l_1^+,l_2]=l_1,
\\
&[l_0,l_2]=-4\alpha_2g_0l_2-(2\alpha_1+4\alpha_2)l_2,
&&[l_2,l_2^+]=g_0,
\\
&[l_0,l_2^+]=4\alpha_2l_2^+g_0+(2\alpha_1+4\alpha_2)l_2^+,
&&[g_0,l_k^{\pm}]=\pm kl_k
.
\end{align}

According to the BRST method of Lagrangian construction (see e.g.
\cite{bkl}) since among the operators (\ref{EM-l0})--(\ref{EM-g0})
there are operators $g_0$, $g_m$ which are not constrains neither in
the space of bra vectors nor in the space of ket vectors then we
must construct extended expressions for the operators
$o_i\to{}O_i=o_i+o_i'$ where $o_i'$ are additional parts to the
initial operators $o_i=\{l_0,l_1,l_1^+l_2,l_2^+,g_0,g_m\}$
(\ref{EM-l0})--(\ref{EM-g0}). These additional parts are constructed
from new (additional) creation and annihilation operators and
commute with the initial operators $[o_i,o_j']=0$. The extended
expressions for the operators must satisfy two conditions: 1)~they
must form an algebra $[O_i,O_j]\sim{}O_k$; 2)~the operators which
are not constraints $g_0$, $g_m$ must be zero or contain linearly
arbitrary parameters which value will be defined later from the
condition of reproducing desired equations of motion.

Using the method elaborated in \cite{bkl} we find algebras of the additional
parts
\begin{align}
\label{EM-l1l1+'}
&
[l_1',l_1^{\prime+}]=-l_0'-g_m'+\alpha_1g_0'-\alpha_2g_0^{\prime2},
\\
&
\label{EM-l1l0'}
[l_1',l_0']=-2\alpha_2g_0'l_1'+(\alpha_1-\alpha_2)l_1',
&&
[l_2^{\prime+},l_1']=l_1^{\prime+},
\\
\label{EM-l0l1+'}
&
[l_0',l_1^{+\prime}]=-2\alpha_2l_1^{+\prime}g_0'+(\alpha_1-\alpha_2)l_1^{+\prime},
&&
[l_1^{\prime}+,l_2']=l_1',
\\
\label{EM-l0l2'}
&
[l_2',l_0']=-4\alpha_2g_0'l_2'+(2\alpha_1-4\alpha_2)l_2',
&&
[l_2',l_2^{\prime+}]=g_0',
\\
\label{EM-l0l2+'}
&
[l_0',l_2^{+\prime}]=-4\alpha_2l_2^{+\prime}g_0'+(2\alpha_1-4\alpha_2)l_2^{+\prime},
&&
[g_0',l_k^{\prime\pm}]=\pm kl_k^{\prime\pm}
\end{align}
and of the extended operators
\begin{align}
&
\label{EM-L1+L1}
[L_1^+,L_1]=L_0+G_m-\alpha_1G_0-\alpha_2G_0^2+2\alpha_2g_0'G_0
\\{}
\label{EM-L1L0}
&
[L_1,L_0]=\alpha_2(G_0L_1+L_1G_0)+\alpha_1L_1
-2\alpha_2g_0'L_1-2\alpha_2l_1'G_0,
&&
[L_2^+,L_1]=L_1^+,
\\{}
\label{EM-L0L1+}
&
[L_0,L_1^+]=\alpha_2(L_1^+G_0+G_0L_1^+)+\alpha_1L_1^+
-2\alpha_2g_0'L_1^+-2\alpha_2l_1^{\prime+}G_0,
&&
[L_1^+,L_2]=L_1,
\\{}
\label{EM-L0L2}
&
[L_2,L_0]=2\alpha_2(G_0L_2+L_2G_0)+2\alpha_1L_2
-4\alpha_2g_0'L_2-4\alpha_2l_2'G_0,
&&
[L_2,L_2^+]=G_0,
\\{}
\label{EM-L0L2+}
&
[L_0,L_2^+]=2(L_2^+G_0+G_0L_1^+)+2\alpha_1L_2^+
-4\alpha_2g_0'L_2^+-4\alpha_2l_2^{+\prime}G_0,
&&
[G_0,L_k^{\pm}]=\pm kL_k^{\pm}.
\end{align}
In RHS of (\ref{EM-L1+L1})--(\ref{EM-L0L2+}) we choose symmetric odering of
the extended operators.
There is a method allowing to construct explicit form of operators in terms
of creation and annihilation operators on the base of their algebra, see e.g.
\cite{bkl} and references therein.
But for our purpose we need no any explicit realization of the additional
parts, except only one observation
\begin{eqnarray}
l_0'=\alpha_1g_0'-\alpha_2g_0^{\prime2}
.
\label{EM-l0'}
\end{eqnarray}

The BRST operator constructed on the base of the algebra of the
extended operators is
\begin{eqnarray}
\tilde{Q}
&=&
\eta_0L_{0}+\eta_1^+L_1+\eta_1L_1^++\eta_2^+L_2+\eta_2L_2^++\eta_{G}G_0
+\eta_MG_m
+\eta_1^+\eta_1({\cal{}P}_0+\mathcal{P}_M)
\nonumber
\\&&
{}
+(\eta_G\eta_1^++\eta_2^+\eta_1){\cal{}P}_1
+(\eta_1\eta_G+\eta_1^+\eta_2){\cal{}P}_1^+
+2\eta_G\eta_2^+{\cal{}P}_2
+2\eta_2\eta_G{\cal{}P}_2^+
\nonumber
\\&&
{}
-\eta_2^+\eta_2{\cal{}P}_G
-\eta_1^+\eta_1\Bigl[\alpha_1+\alpha_2(G_0-2g_0')\Bigr]\mathcal{P}_G
\nonumber
\\&&
{}
+\alpha_2\eta_0\Bigl[
\eta_1^+(L_1-2l_1')-\eta_1(L_1^+-2l_1^{+\prime})
+2\eta_2^+(L_2-2l_2')-2\eta_2(L_2^+-2l_2^{+\prime})
\Bigr]
\mathcal{P}_G
\nonumber
\\&&
{}
+\eta_0\Bigl[\alpha_1+\alpha_2(G_0-2g_0')\Bigr]\Bigl(
\eta_1^+\mathcal{P}_1-\eta_1\mathcal{P}_1^++2\eta_2^+\mathcal{P}_2-2\eta_2\mathcal{P}_2^+
\Bigr)
,
\label{EM-BRST}
\end{eqnarray}

Next step of Lagrangian construction is determination of the
arbitrary parameters which must be contained linearly in the
additional parts $g_0'$ and $g_m'$. For this we decompose the BRST
operator extracting its dependence on ghosts $\eta_G$,
$\mathcal{P}_G$, $\eta_M$, $\mathcal{P}_M$, corresponding to these
operators,
\begin{eqnarray}
\tilde{Q}&=&Q+\eta_G\tilde{G}_0+\eta_MG_M+\eta_1^+\eta_1\mathcal{P}_M+\mathcal{B}\mathcal{P}_G
\end{eqnarray}
where
\begin{eqnarray}
Q
&=&
\eta_0L_{0}+\eta_1^+L_1+\eta_1L_1^++\eta_2^+L_2+\eta_2L_2^+
+\eta_1^+\eta_1{\cal{}P}_0
+\eta_2^+\eta_1{\cal{}P}_1
+\eta_1^+\eta_2{\cal{}P}_1^+
\nonumber
\\&&
{}
+\eta_0\Bigl[\alpha_1+\alpha_2(G_0-2g_0')\Bigr]\Bigl(
\eta_1^+\mathcal{P}_1-\eta_1\mathcal{P}_1^++2\eta_2^+\mathcal{P}_2-2\eta_2\mathcal{P}_2^+
\Bigr)
,
\label{EM-Q}
\\
\tilde{G}_0&=&G_0+
\eta_1^+\mathcal{P}_1-\eta_1\mathcal{P}_1^++2\eta_2^+\mathcal{P}_2-2\eta_2\mathcal{P}_2^+
,
\end{eqnarray}
(explicit expression for $\mathcal{B}$ is not essential)
and suppose that the state vector $|\Psi\rangle$ in the extended space including ghosts
does not depend on ghosts $\eta_G$ and $\eta_M$,
$\mathcal{P}_G|\Psi\rangle=\mathcal{P}_M|\Psi\rangle=0$.
As a result the equation defining physical states $\tilde{Q}|\Psi\rangle=0$
is decomposed into three equations
\begin{align}
&Q|\Psi\rangle=0,
&&\tilde{G}_0|\Psi\rangle=0,
&&G_M|\Psi\rangle=0.
\label{EM-3}
\end{align}
Two right equations in (\ref{EM-3}) are used for determination of the
arbitrary constants in $g_0'$ and $g_m'$ and the left equation in
(\ref{EM-3}) is the equation on physical states.
Note that using (\ref{EM-l0'}) and $L_0=l_0+l_0'$ where $l_0$ is given by
(\ref{EM-l0}) operator $Q$ (\ref{EM-Q}) can be rewritten as
\begin{eqnarray}
Q
&=&
\eta_0\Bigl[\partial^2-m^2+\alpha_1\tilde{G}_0+\alpha_2(G_0-2g_0')\tilde{G}_0\Bigr]
\nonumber
\\&&
{}
+\eta_1^+L_1+\eta_1L_1^++\eta_2^+L_2+\eta_2L_2^+
+\eta_1^+\eta_1{\cal{}P}_0
+\eta_2^+\eta_1{\cal{}P}_1
+\eta_1^+\eta_2{\cal{}P}_1^+
\label{EM-QQ}
\end{eqnarray}
and due to the middle equation in (\ref{EM-3}) all the effects of
the ``constant background fields'' $\alpha_1$ and $\alpha_2$
disappear and we get the model of free higher spin field in
Minkowski space.

To summarize, we have developed the BRST approach to Lagrangian
construction for bosonic totally symmetric higher spin field in
external gravitational, vector and third rank tensor fields.
Assuming that interaction with external fields has massless and flat
space limits we prove that the consistent formulation is possible
only in constant curvature space with no nontrivial coupling to the
third rank tensor and the strength of the vector fields. One can
expect that analogous situation will take place for higher spin
fermionic fields and for any deformation of constant curvature space
by more general background tensor fields. However, the above result
does not concern the field models with spins $\frac{3}{2}$ and $2$
where the BRST construction has the specific possibilities
\cite{brst1} and allows the consistent Lagrangian formulation in
Einstein spaces. Thus, the further development of Lagrangian
construction for free higher spin fields interacting with external
fields is related to search for interaction Lagrangians which
contain the inverse mass terms. Some approaches to such Lagrangians
are given in refs. \cite{consist1,consist2}. Also, it would be
interesting to study the consistency conditions for for recently
formulated conformal higher spin fields \cite{Metsaev} if to couple
them to external fields.

{\bf {Acknowledgements}}. The authors are grateful to Yu.M. Zinoviev
and R.R. Metsaev for discussions of some aspects. The work is
partially supported by the RFBR grant, project No.\ 09-02-00078,
grant for LRSS, project No.\ 3558.2010.2. The work of I.L.B. and
P.M.L. is also partially supported by the RFBR-DFG grant, project
No.\ 09-02-91349 and the DFG grant, project No. 436 RUS 113/669/0-4.

redpajama_set_name: RedPajamaArXiv


In the stage of registration study, our purpose is to find out the safety range of activated coagulation time level in cerebral aneurysm and arteriovenous malformations with hybrid operation.
This study is divided into anticoagulation program in cerebral aneurysm with hybrid operation and anticoagulation program in cerebral arteriovenous malformations with hybrid operation two parts, and each part divide into two stage, on the stage of registration study. This study is a multi-center, single-blind, prospective cohort study. Record the patient's intraoperative activated coagulation time Changes in detail, to observe the effect of activated coagulation time maintenance level on hemorrhage event rate of Intraoperative and postoperative 48 hours, purpose to find out the safety range of activated coagulation time level in cerebral aneurysm and arteriovenous malformations with hybrid operation. On the stage of randomized controlled study. This study is a multicenter, single-blind, prospective, randomized controlled study. Patients is divided into intraoperative standard dose group of Heparin Sodium and low dose group of Heparin Sodium randomly. To observe the effect of different anticoagulation regimens on activated coagulation time safety coverage rate during surgery, and finally develop a scientific and effective intraoperative anticoagulant therapy program.
For cerebral aneurysm with hybrid operation, anticoagulation program is decided by different surgeons based on their experience and record the patient's intraoperative activated coagulation time changes in detail.
For arteriovenous malformations with hybrid operation, anticoagulation program is decided by different surgeons based on their experience and record the patient's intraoperative activated coagulation time changes in detail.
Hemorrhage event include intracranial hemorrhage caused by non-surgical reasons, as well as other organs or parts of the massive bleeding or small bleeding, Including subperitoneal hemorrhage, intraocular hemorrhage, gross hematuria, epistaxis time prolonged or repeated, gastrointestinal bleeding, hemoptysis, subconjunctival hemorrhage, hematoma greater than 5cm, bleeding difficult to control the and so on.
Ischemia event include Cerebral infarction and transient ischemic attack.
All the blood lost during the surgery should be collected and measured.
The investigators chose the patiens from the Tiantan hospital and other hospitals that participated in this study.The patients diagnosed as cerebral aneurysm and arteriovenous malformations,and take part in hybrid operation.
1.All patients undergoing hybird surgery.


邢辰: 2018我国高血压防治攻略(征求意见稿). 中玉势华医学信息导报 2018, 很爱很爱你,关于吃盐的6个问题,这篇文章告诉你!,短发女生19(33).
 China Salt Substitute Study Collaborative G: Salt substitution: a low-cost strategy for很爱很爱你,关于吃盐的6个问题,这篇文章告诉你!,短发女生 blood pressure control among rural Chinesjoy69e. A randomized, co陌友恋约ntrolled trial. Journal of hypertension 2007, 25(10):20姿媚堂化妆品怎样样11-2018.


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redpajama_set_name: RedPajamaGithub


text:
A Sachs–Hornbostel-féle osztályozás a hangszerek osztályozásának Erich Moritz von Hornbostel és Curt Sachs által publikált rendszere, amely először a Zeitschrift für Ethnologie című kiadványban, 1914-ben jelent meg. Ez napjainkban a hangszerek tudományos osztályozásának legelterjedtebb módszere.

Az osztályozás alapjait még a 19. században Victor-Charles Mahillon fektette le, aki a brüsszeli konzervatórium hangszergyűjteményének kurátora volt. Mahillon a hangszereket négy fő kategóriába sorolta elsődleges hangképzésük természete alapján, tehát hogy levegőoszlop, kifeszített húr, membrán vagy a szilárd hangszertest rezgése következtében jön-e létre bennük a hang. Ez a rendszer elsősorban a klasszikus nyugati zenéhez használt hangszereket osztályozta, a Hornbostel–Sachs-rendszertan ezt kibővítve lehetővé tette, hogy szinte bármely zenekultúra akármelyik hangszere a rendszerbe illeszthető legyen.

Formailag hasonlít a könyvtári besorolásra használt Dewey-féle tizedes osztályozásra. Négy fő kategóriája van, azt osztja tovább lépésről lépésre, szintről szintre, minden szinten egy-egy decimális számjegyet rendelve hozzá. Végeredményképpen minden hangszernek így egyértelműen megfeleltethető egy sokjegyű szám.

1 Idiofonok

11 Ütött idiofonok

 111 Közvetlenül ütött
 111.1 Összeütött - kasztanyetta, cintányér, claves
 111.2 Megütött - xilofon, marimba, vibrafon, gong, harang

 112 Közvetve ütött
 112.1 Rázott - maracas, csengettyű
 112.2 Kapart - güiro, kereplő

12 Pengetett idiofonok - lamellofonok

 121 Keretes pengetett - doromb

 122 Fésűs pengetett - zenedoboz

13 Dörzsölt idiofonok

 131 Dörzsölt rudak - tűhegedűk

 132 Dörzsölt lemezek - éneklő fűrész

 133 Dörzsölt edények - hangtálak

14 Fújt idiofonok

 141 Fújt rudak - aeolidon

 142 Fújt lemezek

2 Membranofonok

21 Ütött membranofonok

 211 Közveltlenül ütött
 211.1 Edény alakú - üstdobok
 211.2 Csöves alakú - pergő, tam, konga, bongó
 211.3 Keretes

 212 Rázva ütőtt - damru, den-den-daiko

22 Pengetett membranofonok

 pengetett dobok

(Néhányan úgy tartják, ezen csoportba tartozó hangszerek igazából kordofon hangszerek)

23 Dörzsölt membranofonok

 231 Bottal dörzsölt - köcsögduda
 232 Kötéllel dörzsölt - bika
 233 Kézzel dörzsölt

24 Éneklő membranofonok

 kazoo, nádmirliton, tökmirliton

3 Kordofonok

31 Egyszerű kordofonok – citerák

 311 Rúdciterák - zenélő íj
 312 Csőciterák - kong ring
 313 Tutajciterák
 314 Deszkaciterák - csembaló, zongora, citera
 315 Vályúciterák
 316 Keretciterák

32 Összetett kordofonok

 321 Lantok - nyugati lant, gitár, hegedű, líra
 322 Hárfák - hárfa
 323 Hárfalantok - kora

4 Aerofonok

41 Nyitott aerofonok

 411 Élgerjesztett - pörgettyű, ostor
 412 Szaggatva gerjesztett - harmonika, szájharmonika
 413 Explozív - ceglédi kanna

42 Zárt aerofonok - fúvós hangszerek

 421 Ajaksípok - furulya, fuvola, okarina, körtemuzsika
 422 Nádsípok
 422.1 Kettős nádnyelvesek - oboa, fagot, angolkürt, zurna, duduk
 422.2 Egyszerű nádnyelvesek - klarinét, szaxofon, tárogató
 423 Trombiták - trombita, harsona, tuba, kürt

5 Elektrofonok

51 Elektromos működésű

 elektromos orgona

52 Elektromos erősítéssel rendelkező

 elektromos gitár

53 Radioelektromos

 theremin

Példák
Például a hegedű a következőképpen helyezkedik el a rendszerben:

 3 kordofonok (egy vagy több húr van két pont között kifeszítve)
 32 összetett kordofonok (a hangszer egy húrhordozóból és a szervesen hozzáépült rezonanciatestből áll)
 321 lantok (a húrok a tetővel párhuzamos síkban vannak)
 321.3 nyeles lantok (a húrhordozó egyetlen nyélszerű nyúlvány)
 321.32 nyaklantok (a nyél a testből indul ki)
 321.322 doboz-nyaklantok (a test dobozszerű)
 321.322–7 dörzsöléssel szólaltatják meg
 321.322–71 vonós

Külső hivatkozások
 Az osztályozás eredeti leírása a német wikipédiában
 Erich M. von Hornbostel & Curt Sachs: Systematik der Musikinstrumente. Ein Versuch
 Margaret J. Kartomi. On concepts and classifications of musical instruments – Google könyvek

Hangszerek

redpajama_set_name: RedPajamaWikipedia


text:
alcohol neurotoxicity
Transféré par trappedreflection
enregistrerEnregistrer alcohol neurotoxicity pour plus tard
Bimbingan Koass Neuroimejing
chapter3cv_53226
how family life and status affect visual problems in impoverished communities
Paper 2-Kelas Tambahan
ap frqs brain
Final Voluntry Movement
Characterization of Oligomerization–Aggregation Products of Neurodegenerative Target Proteins by Ion Mobility Mass Spectrometry - Vlad et al. - Intrinsically Disordered Protein Analysis - 2012
Alcohol Consumption Among Young
Org as Brains2
Anatomicamente Ingles
Alzheimer Modelos Animais
2007_sample_essay_handout
ADOLESCENCE - VULNERABLE PERIOD FOR ALCOHOL USE.
Health and Human Services: HowardShapiro
apa lit review 3
description: tags: 2008-184a
Chapter 2: Alcohol and the Brain: Neuroscience and Neurobehavior
The Neurotoxicity of Alcohol
The brain is a major target for the actions of Neuropathologic Changes
alcohol, and heavy alcohol consumption has long
been associated with brain damage. Studies The brain contains as many as 1 trillion nerve
clearly indicate that alcohol is neurotoxic, with cells, or neurons. They come in a variety of
direct effects on nerve cells. Chronic alcohol shapes and sizes, some looking like old oak trees
abusers are at additional risk for brain injury and others like weather balloons. Many of these
from related causes, such as poor nutrition, liver cells project into other brain areas where they
disease, and head trauma. regulate the activity of those areas, thereby
affecting thoughts, consciousness, decisions,
The potential cost to society of alcohol-induced mood, and attention. For every nerve cell in the
brain damage is enormous. Approximately brain that is actively engaged in such things as
14 million Americans—about 7.4 percent of the thoughts, emotions, and movements, there are
adult population—meet the diagnostic criteria for 10 other cells, called glia, that provide important
alcohol abuse or alcoholism (Grant et al. 1994). support to nerve cells. Both of these cell types
On any given day, more than 700,000 people in are damaged by chronic alcohol abuse. Loss of a
the United States receive alcoholism treatment in critical few due to alcohol-induced brain damage
either inpatient or outpatient settings (National may have subtle but important effects on
Institute on Alcohol Abuse and Alcoholism decision-making processes, mood, and behavior.
[NIAAA] 1997). Approximately 9 percent of
alcohol-dependent individuals have clinically There appears to be a continuum of brain damage
diagnosable brain disorders (Eckardt and Martin in long-term alcoholics, progressing from mod-
1986). Indeed, alcoholic dementia is the second- erate deficits in the majority of long-term alcohol
leading cause of adult dementia in the United abusers to the severe psychosis of Wernicke-
States, accounting for 10 percent of cases (Eckardt Korsakoff syndrome (Butterworth 1995; Pfeffer-
and Martin 1986). It is exceeded only by baum et al. 1996). This syndrome includes
Alzheimer's disease. Many studies report that Wernicke's encephalopathy and Korsakoff 's
50 to 75 percent of detoxified long-term alcohol- psychosis, also called Korsakoff 's amnestic
dependent individuals show some degree of syndrome. Wernicke's encephalopathy is
cognitive impairment (Eckardt and Martin 1986), associated with thiamine deficiency resulting
suggesting that brain dysfunction may persist from malnutrition. Prompt treatment with
even after the individual has stopped drinking. massive doses of thiamine may improve
symptoms of this disorder, which include
Individual susceptibility to alcohol-induced brain confusion, ataxia (disordered gait), and visual
damage is highly variable and is related to many abnormalities. Patients have characteristic
factors, such as gender, genetics, environment, brain lesions that may be detected by magnetic
and sociodemographics (Dufour 1993). Suscepti- resonance imaging (MRI). Korsakoff 's psychosis
bility to alcohol dependence is similarly variable; is characterized by anterograde amnesia, where
some people become dependent at much lower the individual is unable to retain new information
levels of consumption than others do. Therefore, (Eckardt et al. 1981). For example, the patient
it is difficult to specify the levels of alcohol views as total strangers people who were encoun-
consumption that are likely to lead to alcohol- tered moments before. The memory dysfunction
induced brain damage. There is a serious need correlates with the presence of lesions in the
for further research in this area. thalamus, a brain structure involved in the
routing of sensory information in the brain
Figure 1: Reduced brain mass in alcoholics
Axial magnetic resonance images from a healthy 57-year-old man (left) and a 57-year-old man with a history of heavy alcohol
consumption (right). Images are courtesy of Dr. Adolf Pfefferbaum.
(Victor et al. 1989). Although these two condi- observations are supported by imaging analyses.
tions usually occur in sequence, they may exist For example, studies using MRI and computed
independently; not all patients with Wernicke's tomography (CT) show enlargement of the
encephalopathy progress to Korsakoff 's psychosis, cerebral ventricles (cavities within the brain
and Korsakoff 's psychosis may occur without a that are filled with cerebrospinal fluid) and
preceding episode of Wernicke's encephalopathy. sulci (furrows on the surface of the cerebrum)
in most alcoholics. Enlargement of these
Extremely heavy alcohol consumption for a structures reflects a shrinkage of brain mass
prolonged period is generally required to produce (figure 1), consistent with postmortem studies
the most severe organic brain disease. One study that show reduced brain weight in alcoholics. In
that compared Wernicke-Korsakoff patients with severe alcoholics, the reductions in weight of the
alcoholics who did not have serious neuro- cerebral hemispheres and the cerebellum (a brain
psychological deficits found that both age of structure predominantly involved in balance and
onset and duration of heavy drinking correlated movement; see figure 2) are significant compared
with the development of Korsakoff 's psychosis with nondrinkers and moderate drinkers (Harper
(Jacobson 1990). Those with Wernicke-Korsakoff and Kril 1993). The reduced brain mass is
syndrome began consuming approximately probably due to a combination of actual loss
12 drinks a day at age 25 and drank at that of nerve cells and reduction in cell size. With
level for 27 years. sustained abstinence for 1 to 5 months, the defect
begins to disappear. This recovery probably
Morphological Changes involves increases in neuronal cell size, number
and size of the supporting glial cells, and arbori-
Postmortem studies of brain tissue in both zation (branching) of nerve endings (Franke et al.
humans and animals suggest that chronic heavy 1997). However, neurons that die are lost forever.
alcohol use changes brain structure. These
Figure 2: Anatomy of the brain
Cerebrum Cortex
Largest portion of the brain, Outer layer of gray matter covering the
including the cerebral surface of the cerebrum and the cerebellum
hemispheres (cerebral cortex
and basel ganglia); involved in
controlling consciousness and Neocortex
voluntary processes Outermost portion of the cerebral
cortex that contains the most
Corpus callosum structurally complex brain tissue
A bundle of fibers connecting
the brain's hemispheres Diencephalon
Hippocampus • Septal area–related to the
Part of the limbic system, which limbic system, which is
is involved in emotional aspects involved in emotional
of survival behavior; also plays aspects of survival behavior
a role in memory • Thalamus–a
communication center that
Basal ganglia relays information to the
A group of structures lying deep cerebral cortex
in the brain involved in • Hypothalamus–important in
movement and cognition maintaining the body's
Cerebellum
Involved in maintenance internal environment, or
of posture, balance, and homeostasis, through the
coordination receipt of sensory and
chemical input
Source: Mattson et al. 1994.
Data from tissue and quantitative morphometry developed in humans; among its functions, it is
(structural) studies demonstrate selective neuronal the center for intellectual capacity.) Alcoholics
loss, reduced arborization, and reduction of with severe brain disorders, such as Wernicke-
synaptic complexity in specific brain regions of Korsakoff syndrome, show more significant
alcoholics. The frontal lobes (of the cerebrum)— reduction in white matter and more extensive
whose functions encompass the initiation of brain degeneration than do alcoholics with less
motor activity and the integration of behavior, severe disorders.
intellect, and emotion—appear to be particularly
sensitive to alcohol-induced changes (Jernigan et Investigators have found a 22-percent reduction
al. 1991). They show the greatest decrease in in the number of neurons in the superior frontal
mass and account for much of the associated cortex and motor cortex of alcoholics compared
ventricular enlargement. Both gray matter, which with nonalcoholic controls, but no significant
is composed largely of neurons, and white matter, differences in other areas of the cortex (Harper
which is composed of myelinated nerve fibers, et al. 1987). Recent studies of alcoholics have
appear to be decreased. (The myelin sheath reported a relationship between temporal lobe
around nerve fibers facilitates the conduction of shrinkage and a history of alcohol withdrawal
nerve impulses.) There appears to be a selective seizures, while frontal lobe shrinkage occurs in
loss of white matter, particularly in the frontal alcoholics regardless of their seizure history
lobes, but it is uncertain how the observed (Sullivan et al. 1996). A decrease in the amount
cellular lesions relate to this loss. One reason of N-acetylaspartate in the frontal lobe, a measure
these changes are more evident is the greater of neuron viability, is another indication of fron-
proportion of white matter to cortical gray matter tal lobe degeneration in alcoholics (Jagannathan
in the frontal regions. (Cortical refers to the et al. 1996). The findings of severe damage to
cerebral cortex, a thin layer of gray matter on the the frontal cortex in alcoholics are consistent with
surface of the cerebrum. It is most extensively clinical and neuroradiological findings, which
suggest that the frontal lobe may be more the brain, including the regulation of mood
susceptible than other cortical regions to alcohol- states, thinking patterns, appetite, sleep, and
induced brain damage. The large neurons that even behavior, such as alcohol drinking. The
are lost in this frontal region (the pyramidal serotonergic system appears to be disrupted in
neurons) are also recognized as being more alcoholics, particularly in severe alcoholics (Baker
vulnerable in Alzheimer's disease and as part et al. 1996; Halliday et al. 1995). Recent studies
of the normal aging process. of alcoholics have found a reduction of up to
50 percent in the number of serotonergic neurons
Recent studies have found that in addition to from both these raphe nuclei compared with
the global shrinkage of brain regions, neurons in nonalcoholic controls. Further, chemical studies
certain structures called nuclei are selectively lost have shown abnormally low levels of serotonergic
with chronic alcohol abuse. Nuclei are clusters metabolites in the cerebrospinal fluid of alcoholics
of neurons that have broad-ranging functions in with Wernicke-Korsakoff syndrome.
brain activity; they are distinguishable by cell type
or by clear demarcation from the surrounding Specific types of brain cells appear to be dis-
tissue. Perhaps the most extensively studied rupted. Recent studies have indicated that certain
nuclei are the cholinergic nuclei in the basal neurons containing the peptide vasopressin may
forebrain. Neurons within these nuclei are be sensitive to chronic alcohol-induced neuro-
involved with the production and release of toxicity in both humans and animals (Harding et
acetylcholine, a neurotransmitter associated with al. 1996; Madeira et al. 1997). Vasopressin is a
many important physiologic functions. Both hormone that is involved in the regulation of
human and animal studies suggest that this both physiologic processes and neurobehavioral
region is particularly susceptible to damage in function. Damage to neurons containing
alcoholic subjects. Researchers have reported that vasopressin and other peptides could disrupt a
Korsakoff 's psychosis causes both neuronal loss variety of hormone functions as well as the daily
and shrinkage in this area, with one study rhythms that are important for healthy living.
reporting a significant loss of neurons (Arendt Further studies are needed to determine whether
1993). Neurons in the cholinergic nuclei are also additional specific cell groups within the brain are
lost in Alzheimer's disease. particularly susceptible to damage. Neuronal loss
in small but functionally significant brain areas
Other brain nuclei that appear to be particularly could result in global changes in attention, mood,
sensitive are the locus ceruleus and the raphe and personality that are difficult to quantify but
nuclei. These nuclei are small but important have a great impact on brain function and overall
because their neuronal processes project through- behavior.
out the brain and modulate global aspects of
brain activity. For example, lesions in the locus Recent animal studies have found that long-term
ceruleus, which contains many of the noradren- alcohol intoxication is not necessary for brain
ergic neurons (those that secrete the neuro- damage to occur. As little as a few days of
transmitter norepinephrine) in the brain, may intoxication can lead to neuronal loss in several
impair attention and information processing and specific areas of the cerebral cortex (Collins et al.
may affect learning and memory. Several studies 1996). These findings are consistent with recent
have reported significant noradrenergic cell loss in studies in human alcoholics that report damage to
the locus ceruleus (Arango et al. 1996; Arendt et one of these cortical areas (Ibanez et al. 1995) and
al. 1995; Lu et al. 1997), but not all studies have significant shrinkage of the hippocampus, an area
found this loss (Harper and Kril 1993). The involved in learning and memory (Harding et al.
median and dorsal raphe nuclei together provide 1997). Chronic alcohol treatment of animals has
the primary source of serotonergic axons in the shown that hippocampal damage is correlated
cerebral cortex. These neurons secrete serotonin, with deficits in spatial learning and memory
a neurotransmitter that affects multiple actions in (Franke et al. 1997). These studies indicate that
cortical and hippocampal damage can occur in Alcoholics who do not suffer from Wernicke-
animals with both chronic and short-term Korsakoff syndrome still show greater loss of
alcohol exposure. This suggests that, in humans, neuropsychological performance than peer
relatively short durations of alcohol abuse are nonalcoholics do on tests of learning, memory,
likely to cause some form of damage. abstracting, problem solving, visuospatial and
perceptual motor functioning, and information
Exciting new studies have begun to address the processing (Parsons 1993). Alcoholics are less
effects of gender on alcohol-induced brain accurate and take considerably longer to complete
damage. Interestingly, alcoholic women appear tasks. Many of the deficits appear to recover to
to have an increased sensitivity for brain damage age-appropriate levels of performance after 4 to
compared with alcoholic men (Hommer et al. 5 years of abstinence (Parsons 1993). However,
1996). This difference appears to be true for liver even though global cerebral atrophy may return
and heart damage as well. Although more men to near normal levels with extended abstinence,
than women are diagnosed as alcoholic, the not all cognitive functions return. Some
number of alcoholic women is increasing. abstinent alcoholics appear to have permanent
Therefore, the increased susceptibility of women cognitive impairments, particularly in memory
to alcoholic brain damage is an area that needs and visual-spatial-motor skills (Di Sclafani et al.
further investigation. 1995). Other studies support a loss of logical
memory and paired-association learning tasks in
Functional Changes alcoholics that may be long lasting (Eckardt et al.
Chronic alcohol abuse clearly leads to changes
in brain function, with the degree of dysfunction Recent studies have emphasized the role of the
dependent upon the duration and amount of prefrontal cortex in executive cognitive function
alcohol consumed. Many brain functions related (ECF) (Hoaken et al. 1998). This is the ability
to the frontal cortex appear to be affected. Pre- to use higher mental processes such as attention,
frontal (the most anterior part of the cortex) planning, organization, sequencing, abstract
damage typically is associated with changes in reasoning, and the use of external and internal
personality and cognitive abnormalities. Although feedback to adaptively shape future behavior
these types of changes in brain function are more (Foster et al. 1994). ECF processes are dysfunc-
difficult to assess than physical changes, they tional in alcoholics and in persons with other
are consistent with the morphological changes diseases showing prefrontal damage (Boller et al.
found in the frontal cortex of alcoholics. 1995). Changes in ECF and prefrontal cortical
characteristics are associated with decreased
Both clinical and experimental studies support regulation of human social behavior, including
a role for frontal cortical involvement in neuro- disinhibition syndrome, which is characterized by
psychological deficits in alcoholics, particularly impulsivity, socially inappropriate behavior, and
those with Korsakoff 's psychosis (Oscar-Berman aggression (Giancola and Zeichner 1995a).
and Hutner 1993). These deficits include Disruption of ECF has also been implicated
dysfunction in emotional control, problem- in the underlying aggression associated with
solving ability, and attention. Electrophysiologic substance abuse (Giancola and Zeichner 1995b).
studies using electroencephalograms and event-
related potentials have suggested that alcoholics Mechanisms of Action
have difficulty differentiating relevant and
irrelevant, easy and difficult, and familiar and Researchers have only recently begun to elucidate
unfamiliar stimuli (Porjesz and Begleiter 1993). the mechanisms involved in the neurotoxic effects
These deficits appear to be consistent for alco- of alcohol on the brain. As research techniques
holics and may be related to frontal cortical have become more sophisticated and data from
function. experimental and clinical studies have accumu-
lated, however, investigators have had a more
substantial basis for speculation as to the nature The administration of an antagonist to NMDA
of these mechanisms. receptors, such as MK-801 (dizocilpine), elimi-
nates both alcohol tolerance (Khanna et al. 1992;
NMDA Receptor Supersensitivity Szabo et al. 1994) and withdrawal seizures (Grant
et al. 1990), as well as blocks NMDA-stimulated
One promising avenue of research involves the neuronal death (Chandler et al. 1993a). In
interaction between glutamate, an amino acid animal studies using thiamine-deficient rats as a
that is the major excitatory neurotransmitter model for Wernicke's encephalopathy, extra-
in the brain, and a specific glutamate receptor, cellular concentrations of glutamate in the brain
the N-methyl-D-aspartate (NMDA) receptor. increased several fold during seizures (Langlais
Glutamate and the NMDA receptors are and Zhang 1993). Administration of the NMDA
extensively discussed in other sections of this receptor antagonist MK-801 reduced the neuro-
chapter. The NMDA receptor is inhibited by biological symptoms and the severity of neural
alcohol at a greater level of sensitivity than is any lesioning in these animals (Langlais and Mair
other known glutamate receptor. The acute 1990). These studies and others provide evidence
alcohol-induced inhibition leads to adaptive that NMDA receptor supersensitivity may con-
changes in the NMDA receptor that make it tribute to alcohol tolerance, dependence, and
supersensitive to glutamate during chronic neurotoxicity and to the hyperexcitability and
alcohol exposure. seizures associated with alcohol withdrawal.
However, further research is needed in this area.
Excessive stimulation of NMDA receptors by
glutamate can kill neurons, and chronic alcohol Hyperexcitability of the central nervous system
exposure increases sensitivity of neurons to is a key component of alcohol withdrawal.
NMDA-stimulated killing (Chandler et al. 1993a; A supersensitive glutamate-NMDA response
Crews and Chandler 1993; Iorio et al. 1993). appears to be involved, although a reduction in
Excitotoxicity is a term applied to the direct lethal gamma-aminobutyric acid-mediated inhibition
damage to neurons in extreme cases of excessive also may contribute to this hyperexcitability
glutamate receptor activity, usually accompanied (Crews et al. 1996). (Gamma-aminobutyric acid
by an excessive accumulation of intracellular is a neurotransmitter that inhibits the activity of
calcium ions. This neurotoxic property of the nerve cells.) One of the earliest findings suggest-
receptors appears to play a key role in neuro- ing glutamate involvement was the increased
degenerative diseases in general, as well as in binding of radioactively labeled glutamate
stroke, brain trauma, and other types of brain ([3H]glutamate) in the hippocampus of alcoholics
damage (Crews et al. 1996). The extreme neuro- (Michaelis et al. 1990). Although it is not clear
degeneration associated with Wernicke's which subtype of glutamate receptor is involved,
encephalopathy also appears to involve increases this finding is consistent with increased glutamate
in glutamate-NMDA excitotoxicity. Several receptor density and sensitivity.
studies using cultured neuronal cells have
indicated that a few days of chronic alcohol The mechanisms of NMDA receptor supersen-
treatment lead to supersensitive NMDA receptor- sitivity are not fully understood, but it is clear
stimulated calcium flux (an increase in the that chronic alcohol administration can induce
intracellular concentration of calcium ions) this supersensitivity. This supersensitivity could
(Ahern et al. 1994; Iorio et al. 1992), as well occur through a number of mechanisms, in-
as NMDA receptor-stimulated excitotoxicity cluding an increase in the density of NMDA
(Chandler et al. 1993b; Crews and Chandler receptors, changes in the NMDA receptor
1993; Crews et al. 1993; Iorio et al. 1993) subunit composition, or chemical changes in the
and NMDA receptor-stimulated nitric oxide NMDA receptor that could change its sensitivity.
formation (Chandler et al. 1997). All of these Some, but not all, studies have found increases in
reactions lead to severe neuronal damage. NMDA receptor density. These results, although
inconclusive, suggest that this may be one of the overproduction of free radicals, the result is oxida-
mechanisms underlying chronic alcohol-induced tive stress. This imbalance between increased
NMDA receptor supersensitivity (Chandler et al. production of free radicals and decreased avail-
1997; Crews et al. 1996; Rudolph et al. 1997). ability of antioxidants can result in cell death.
Free radicals also may attack lipids in cell
A second mechanism for inducing NMDA membranes, causing lipid peroxidation. This
receptor supersensitivity could involve changes in is a reaction between oxygen radicals and
the subunit composition of the receptor. The components of the cell membrane that results
NMDA receptor is thought to be made up of five in membrane injury and eventual cell death.
subunits, and changes in the type of subunit
could change NMDA receptor supersensitivity. Studies examining the effects of both acute
Studies have reported that the number of subunits and chronic alcohol administration on cellular
expressed during chronic alcohol exposure is oxidation in the rat brain have focused primarily
altered (Follesa and Ticku 1995, 1996). on alcohol's effects on the activity of antioxidants,
such as alpha-tocopherol, ascorbate, glutathione,
Other studies, however, found alcohol-induced catalase, and superoxide dismutase (Ledig et al.
NMDA receptor supersensitivity without subunit 1981; Montoliu et al. 1994; Nordmann 1987;
changes (Chandler et al. 1997), suggesting that Rouach et al. 1987), or on potential sources of
other mechanisms, such as phosphorylation, oxidative radicals. One of these sources is nitric
might be involved. This is a chemical reaction oxide, which has been implicated in neuronal
that is involved in regulation of receptor activity. toxicity resulting from the formation of highly
Enzymes that phosphorylate (add phosphate to) oxidative metabolites (Crews and Chandler
amino acid residues within the NMDA receptor, 1993). Another source of oxidative radicals is
including tyrosine kinases such as Fyn tyrosine cytochrome P450 2E1, an enzyme that
kinase, may affect NMDA receptor sensitivity metabolizes alcohol and is a potent generator of
during alcohol treatment (Miyakawa et al. 1997). these radicals (Montoliu et al. 1994, 1995).
These mechanisms could occur as a continuum, Increases in cytochrome P450 2E1 and other
with phosphorylation causing initial supersen- oxidases induced in rats by chronic alcohol
sitivity, and more prolonged and excessive alcohol administration have been related to increased
consumption causing additional supersensitivity lipid peroxidation and the formation of reactive
through changes in subunits and slight increases oxygen radicals in the brain (Montoliu et al.
in NMDA receptor density. Because of the 1994). However, levels of antioxidant enzymes,
consistent finding that NMDA supersensitivity such as catalase and superoxide dismutase, appear
during chronic alcohol treatment leads to to increase as a compensatory mechanism
increased NMDA receptor-stimulated neuronal (Montoliu et al. 1994).
excitotoxicity, all of these mechanisms are being
further investigated. The brain is particularly susceptible to lipid
peroxidation because it consumes a large amount
Oxidative Stress of oxygen and is rich in polyunsaturated fatty
acids, which are particularly prone to injury from
Another possible mechanism for alcohol-induced oxygen radicals. Experiments with cells of rat
brain damage involves oxidative stress of neurons. brains have shown that a single dose of alcohol
As a by-product of alcohol metabolism, free results in both increases in lipid hydroperoxide
radicals may be formed. These are highly reactive levels and decreases in glutathione levels (Nord-
molecular fragments that are capable of inflicting mann et al. 1990, 1992; Uysal et al. 1986, 1989).
serious damage on cells if they are not quickly It is not clear whether or how this increased
neutralized. Normally, free radicals are rapidly oxidation is associated with increased brain
inactivated by antioxidants, which are protective damage. Most studies have focused on whole-
molecules that inhibit oxidation. However, if brain homogenates, rather than on cells of specific
these defenses are impaired, or if there is an brain regions. However, a recent study of
alcohol-induced depression of glutathione and possibility that growth factors may be used to
glutamine synthetase levels, two indices of treat alcohol-induced brain damage as well as
increased oxidative radical formation, used cells other neurodegenerative conditions. Studies of
from specific brain regions. Researchers found the actions of growth factors and of their role
changes only in cells from the striatum (a center in alcohol-induced brain damage represent an
involved in the programming of movement), but exciting new area of discovery that could provide
not in cells from the cerebral cortex or cerebellum new approaches to treatment of neurodegener-
(structures involved in balance and motor ation.
coordination) (Bondy and Guo 1995).
Oxidative stress has been implicated in the effects
of aging and in a variety of neurodegenerative Alcoholism is a progressive disease that starts
disorders, such as Alzheimer's disease, Parkin- with experimentation and progresses to addiction,
sonism, and stroke. Much more research on usually over the course of several years. Addiction
alcohol-induced neurodegeneration is needed to involves the loss of control over the ability to
provide a more complete understanding of how abstain from the drug and an excessive preoccupa-
oxidation damages neurons and how other brain tion with obtaining and using the drug. Discov-
cells respond to increased oxidative stress. eries continue to unravel structure-function
Alcohol-induced neurodegeneration may be aspects of the brain and suggest that some of the
related to an induction of oxidative enzymes; behavioral problems of alcoholism may be related
alcohol research provides an opportunity to to alcohol-induced damage to specific brain areas.
clearly address this aspect of neurodegeneration, While earlier studies focused on alcohol-induced
which could impact a broad range of diseases. changes in cognition, more recent studies are
focusing on the frontal cortex, which is partic-
ularly sensitive to alcohol-induced damage,
Growth Factors and on the role of this brain region in behavior.
Growth factors are specific protein elements of Experimental subjects with poor prefrontal
the brain that stimulate growth and extensions functioning appear unable to inhibit impulsive
of neurons and that are essential to neurons behavior (Lau and Pihl 1996), particularly
for their survival and maintenance of normal violence (Lau et al. 1995). Results of neuro-
function. Growth factors also are known to imaging studies also indicate that reduction of
increase the activity of neuronal antioxidant and metabolic functions in the frontal lobes is
excitotoxic protective mechanisms. The growth associated with violence (Raine et al. 1994).
factors include, among others, nerve growth
factor (NGF), brain-derived neurotrophic factor Taken together, these studies suggest that some of
(bDNF), neurotrophin 3 (NT-3), and basic the greatest sociopathic problems of alcoholism,
fibroblast growth factor (bFGF). such as violence and loss of control over the drug,
may be directly related to the neurotoxic effects
Researchers have found that alcohol alters brain of alcohol on prefrontal cortical function. This
levels of growth factors in rats (Arendt et al. is a particularly exciting hypothesis, because it
1995; Baek et al. 1996; MacLennan et al. 1995; suggests that it may be possible to detect
Nakano et al. 1996). Recent studies have found individuals at risk for addiction through studies
that chronic alcohol administration reduces the of their brain function and to determine whether
level of bDNF but does not change the levels recovery of normal function is associated with the
of NGF, NT-3, or bFGF (Baek et al. 1996; ability to sustain abstinence. Identification of
MacLennan et al. 1995). Receptors for the these individuals would allow focused efforts at
growth factors remain intact after chronic alcohol prevention and education, with the aim of
abuse (Arendt et al. 1995; MacLennan et al. preventing addiction and its accompanying
1995). This finding presents the promising sociopathic behaviors.
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Matev / Mathew 24 : 14 - Ani sotachi sakxi sogllea porzank mellchê khatir hem Sorginchea Rajeachem Xubhvortoman ak'khea sonvsarant porgôtt zatolem. Ani tea uprant xevôtt ietolo. / And this gospel of the kingdom will be preached throughout the world as a witness to all nations, and then the end will come.
Stotranchem Pustok / Psalms 34 : 8 - Sorvesporachi bhokti kortoleank Tacho dut veddho ghalun rakhta. Chakun gheiat ani polleiat: Sorvespor kitlo mhonvall gôdd! Tachea gopant asro sôdta to monis bhagi! / The angel of the LORD encamps around those who fear him, and he saves them. Taste and see that the LORD is good; blessed is the stalwart one who takes refuge in him.
Ezekiel / Ezekiel 3 : 1 - 3 - Tannem mhaka mhollem: 'Mon'- xachea puta, tujê mukhar asa tem kha; ho kovllo kha; magir voch ani Israelachea Ghorannea kodde uloi.'2 Hanvem mhojem tondd ugôddlem; Tannem mhaka to kovllo khaunk dilo. 3 Magir Tannem mhollem: 'Hanv tuka ditam tea kovllean tujem pott bhôr ani dhadoxi za.' Hanvem to khelo ani to mhojea tonddant mhonva itlo gôdd zalo. / He said to me: Son of man, eat what you find here: eat this scroll, then go, speak to the house of Israel. 2 So I opened my mouth, and he gave me the scroll to eat. 3 Son of man, he said to me, feed your stomach and fill your belly with this scroll I am giving you. I ate it, and it was as sweet as honey in my mouth.
Stotranchem Pustok /Psalms 119 : 103 - Tonddant godd-godd mhonva poros odik ruchik Tujea utrachi goddsann mhojea kallzak! / How sweet to my tongue is your promise, sweeter than honey to my mouth!
Mark / Mark 16 : 15 - Ani Tannem tankam sanglem: Ak'khea sonvsarak vochat, sogllê rochnnek Xubhvortoman porgôttat. / He said to them, "Go into the whole world and proclaim the gospel to every creature.
Dhormdutancho Itihas / Acts 4 : 18- 21 - Tankam bhitôr apoun, Jezuchea Nanvan koxêch bhaxen anink uloina zaunk ani xikovnn dina zaunk tãnnim tankam formailem. 19 Punn Pedrun ani Juanvan portipallun mhollem: Tumkam aikun Devak aikona zaunk, hem Devachea dolleam mukhar sarkem zalear tumich nirnnoi diat. 20 Ami kitem dekhlam ani aikolam tem porgôtt korinastana amchean ravunk zaina. 21 Tãnnim tankam anink êk pavtt dhomkaile ani sôddle; khõichêch vatten tankam khast lavunk mellonasli, kiteak sogllo lôk ghòddlam tachê khatir Devak vakhanntalo. / So they called them back and ordered them not to speak or teach at all in the name of Jesus. 19 Peter and John, however, said to them in reply, "Whether it is right in the sight of God for us to obey you rather than God, you be the judges. 20 It is impossible for us not to speak about what we have seen and heard." 21 After threatening them further, they released them, finding no way to punish them, on account of the people who were all praising God for what had happened.
1 Juanv / 1 John 1 : 1 - 5 - Jivitachea Sobda vixim ho amcho sondêx: To orombak thaun aslo, Taka ami aikola ani amcheach dolleamnim dekhla, Taka ami tellun pollela. Taka ami amcheach hatamnim sanspila. 2 Khorench, Jivit dixtti poddlem, Tem ami dekhlam ani Taka ami govai ditanv. Bapa sovem aslem ani Tannench amkam dokhol kelam tem Sasnnik Jivit ami tumkam porgôtt'tanv. 3 Tumi-i amchea ekcharant aschê khatir, jem ami pollelam ani aikolam tench ami tumkam-i kollit kortanv. Amcho ekchar mhollear Bapa kodde ani Tachea Puta Jezu Krista kodde. 4 Amam-somestancho sontôs purnn zaunchê khatir, hem ami tumkam boroitanv. 5 Tachê koddso ami aikola ani tumkam ami porgôtt kortanv to sondêx ho: Dev mhollear Uzvadd ani Tachê sovem kosloch kallôkh na. / What was from the beginning, what we have heard, what we have seen with our eyes, what we looked upon and touched with our hands concerns the Word of life— 2 for the life was made visible; we have seen it and testify to it and proclaim to you the eternal life that was with the Father and was made visible to us—3 what we have seen and heard we proclaim now to you, so that you too may have fellowship with us; for our fellowship is with the Father and with his Son, Jesus Christ. 4 We are writing this so that our joy may be complete. God is Light. 5 Now this is the message that we have heard from him and proclaim to you: God is light, and in him there is no darkness at all.
Juanv / John 18 : 37 - 38 - Pilatan Taka mhollem: Mhonnttôch, raza tum? Jezun zobab dilo: Hanv Raza mhonn tunvench sangleim. Heach pasot Hanv zolmolam, heach pasot sonvsarant ailam: sotak govai diunk. Jim konn sot manun gheunk toiar asat, tim Mhozo tallo aikotat. 38 Pilatan Taka vicharlem: Sot mhonngê kitem? Oxem uloun, novean Judevam sorxem bhair vochun, tankam mhollem: Mhaka tacho kosloch guneanv mellona. / So Pilate said to him, "Then you are a king?" Jesus answered, "You say I am a king. For this I was born and for this I came into the world, to testify to the truth. Everyone who belongs to the truth listens to my voice." 38 Pilate said to him, "What is truth?" When he had said this, he again went out to the Jews and said to them, "I find no guilt in him.
Lukas / Luke 1 : 35 - 38 - Ani devdutan zap diun mhollem: Povitr Atmo tujer ietolo ani Bhov Vortea Devachi xokti tujer savlli ghaltoli. Heach khatir tum zolm diunchi asai tea povitr bhurgeak Devacho Put mhonn Sorvespor nanv ditolo. 36 Ani polle, tujê soirê Elizabetin utar piraier eka putacho gorbh samball'la ani vanztti mhonnttalim ti atam sovea mhoineachi asa. 37 Kiteak Devachean zaina mhonnlolem kãich na. 38 Tednam Marien mhollem: Hi asam hanv Sorvesporachi chakorn: zaum mhojê sovem tujea utra pormannem. Ani devdut tichê sorxilo koddsorlo. / And the angel said to her in reply, "The holy Spirit will come upon you, and the power of the Most High will overshadow you. Therefore the child to be born will be called holy, the Son of God. 36 And behold, Elizabeth, your relative, has also conceived a son in her old age, and this is the sixth month for her who was called barren; 37 for nothing will be impossible for God." 38 Mary said, "Behold, I am the handmaid of the Lord. May it be done to me according to your word." Then the angel departed from her.
Lukas / Luke 2 : 8 - 10 - Teach kheddea ganvant rat-paro korun gonvlli aple hindd rakhtale. 9 Sorvesporacho êk dut tanchê sorxem ubo zalo ani Sorvesporachem tez tanchê bhonvtim porzoll'lem ani te bhieun thorthorle. 10 Devdutan tankam mhollem: Bhieum nakat! Polleiat, vhodda sontosachi khobor hanv tumkam gheun ailam, ani hoch sontôs sogllê porjek bhògtolo; / Now there were shepherds in that region living in the fields and keeping the night watch over their flock. 9 The angel of the Lord appeared to them and the glory of the Lord shone around them, and they were struck with great fear. 10 The angel said to them, "Do not be afraid; for behold, I proclaim to you good news of great joy that will be for all the people.
Romkarank / Romans 10 : 15 - 17 - Ani tankam dhaddlea xivai porgôtt kortolim koxim? Tôr Povitr Pustokar oxem boroilolem asa: Xubh khobor porgôtt'tat tanchim panvlam kitlim sobit! 16 Punn xubh khobor sogllinch manun ghenant. Dekhunuch Izaias mhonntta: Sorvespora, ami porgôttlam tem konnem manun ghetlam? 17 Mhonnttôch Kristacho sondêx kanar poddcho; ani to kanar-poddun, bhavarth utpon zauncho. / And how can people preach unless they are sent? As it is written, "How beautiful are the feet of those who bring [the] good news!" 16 But not everyone has heeded the good news; for Isaiah says, "Lord, who has believed what was heard from us?" 17 Thus faith comes from what is heard, and what is heard comes through the word of Christ.
Romkarank / Romans 1 : 16 - Xubhvortomanacho mhaka purnn visvas asa, kiteak Xubhvortoman bhavarth dhôrtolea sogllea mon'xank taronn diupi Devachi xokti: poilim Judevank, uprant Grikank-ui. / For I am not ashamed of the gospel. It is the power of God for the salvation of everyone who believes: for Jew first, and then Greek.
Koloskarank / Colossians 3 : 11 - Hantum anink Grik ani Judêv mhonn na, sunôt kel'lo ani sunôt na-kel'lo mhonn na, porko ani zonglli monis mhonn na, gulam' ani svotontr monis mhonn na. Asa to ekloch Krist soglleam sovem Toch! / Here there is not Greek and Jew, circumcision and uncircumcision, barbarian, Scythian, slave, free; but Christ is all and in all.
Juanv / John 8 : 31 - 32 - Apnnacher bhavarth dovorlo tea Judevank Jezun mhollem: Tumi Mhojem utor tumchê bhitôr rigun dovorxat zalear, tumi khoreponnim Mhoje xis zatoleat. 32 Ani tumkam sot kollon ietolem ani sot tumkam svotontr kortolem. / Jesus then said to those Jews who believed in him, "If you remain in my word, you will truly be my disciples, 32 and you will know the truth, and the truth will set you free.
Izaias / Isaiah 6 : 7 - 8 - Tannem to mhojea onttank lailo ani mhollem: 'Polle, ho tujea onttank laila, tuzo guneanv kaddun uddoilo, tujem patok bhogsolem. 8 Tedna Sorvesporacho tallo hanvem aikolo; to oxem mhonnttalo: 'Konnak dhaddum? Amchea nanvan vochunk konn asot?' / He touched my mouth with it. "See," he said, "now that this has touched your lips, your wickedness is removed, your sin purged." 8 Then I heard the voice of the Lord saying, "Whom shall I send? Who will go for us?" "Here I am," I said; "send me!