Thuja occidentalis
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Cupressaceae
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Tree
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Arbor Vitae
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The Od Force of the leafy branches
is used as one of the components in the preparation of the remedy. As herbal it
is non-poisonous.
The Od Force sweeps the dangerous
toxic attributes of the GABA (gamma aminobutyric acid) receptor antagonistic. In this
capacity it reverses the sufferings of asthma attack, intestinal irritation,
excess stimulation of the nervous system and spontaneous abortions
(miscarriage). It withdraws the spasm, caused seizures as well as the damages
of the liver and the kidneys. It cancels the poisoning. In respect of the skin
or eye it lifts the severe irritation and burns. It cures the rashes, skin
diseases, warts if it is within its capacity. People with seizure disorders or
gastrointestinal problems like ulcers or gastritis welcomes this force
unknowingly.
It
lifts the diversions caused from the chemically treated bronchitis, skin
infections, cold sores and cancer. The diversion caused from the chemically
treated pains of the osteoarthritis, joints and muscles. It lifts the focus
newly appeared due to chemically ordered the nerve disorder of the trigeminal
neuralgia affecting the face as this made order is caused at the cost of loss
of further loss from the remaining fund of the Od Force of the suffering human
system. Immunostimulant boosting over the immune system to loose the phlegm as
an expectorant is withdrawn by this Od Force. It erases the diversions caused
from brain
problems.
It
is peculiarly equipped to stop the queasiness, vomiting, painful diarrhea to
death.
If the immune system is made too active then
this activation may increase the symptoms of autoimmune diseases. And such
diseases of multiple sclerosis (MS), lupus (systemic lupus erythematosus, SLE),
rheumatoid arthritis (RA) and other conditions are the subjects of this Od
Force. It also bats for some serious side effects caused chemically. The
diversion caused further in the tackling or in decreasing the toxic effects of
chemotherapy and radiation therapy is withdrawn as this Od Force is
administered. The chemical treatment of the throat and the respiratory distress
gunned to the congestive heart failure is vanquished in the use of this Od
Force. The damaged done due to chemically diuretic increase of urination and
chemical astringency applied to purify the blood, to reduce inflammation to
cleanse the body of toxins cause harm in some new zone of the human system as
these chemicals function only at the cost of the further subtraction of the
previous fund of the pretreated condition and naturally this Od Force in its
capacity lifts the system from the depth of additional loss of the Of Force.
In the process of inhibiting metastasis of tumor
cells cell-mediated immune system is stimulated and pro-inflammatory cytokines
is decreased. The Od Force in question to reverse the diversion caused from the
said inhibition in the result of the said stimulation of the cells
cell-mediated immune system and pro-inflammatory cytokines decrease, vibrates
the cell to cell electromagnetic network of the said suffering human system
that adds the deficient Od Force which had been lost during the process of the
said inhibition and hereby the pre-inhibition condition is reched. In this
reversing process all of the cytotoxic T-lymphocyte (CTL) activity, natural
killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC)
and antibody-dependent complement-mediated cytotoxicity (ACC), pro-inflammatory
cytokines and tissue inhibitor matrix metalloproteinases (TIMP) walk back. Enhanced
the NK cell activity, ADCC and ACC much earlier than the control tumor, are
withdrawn. It causes increase in the decreased elevated level of
pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, GM-CSF and tumor
necrosis factor (TNF)-α. The elevated level of antitumor factors such as IL-2
and TIMP are alco decreased. Thus previous immune surveillance is
reestablished.
Mitogenic and cluster-forming activity causes T
cell induction, in particular, of CD 4-positive T-helper/inducer cells as
opposed to B cells. The CD-4+ T-helper/inducer cell induction is connected to
an increased production of IL-2. The Od Force in question here reverses the
total process if it is in its capacity. It may lift the induction over the CD4+
fraction of the peripheral blood T-cell subset. It is a potent exhibitor of the
inhibited expression of HIV-1-specific antigens and HIV-1-specific reverse
transcriptase. It may reverse the cytokine pattern induced in peripheral blood
lymphocytes (PBL) and monocyte /macrophage cultures. It may withdraw the induction
over IL-1 beta, IL-2, IL-3, IL-6, gumma-IFN, G-CSF, GM-CSF and TNF-beta
production in PBL cultures and IL-1 beta, IL-6 in monocyte /macrophage
cultures.
GABA is a chemical messenger that is widely distributed in the
brain. Its natural function is to reduce the activity of the neurons to which
it binds.It is the brain’s main inhibitory neurotransmitter. Some medications
can enhance the natural reducing neural effect of GABA. It is estimated that close to 40% of the synapses in the brain work with
GABA and therefore have GABA receptors. GABA receptors are channel
receptors. This means that when GABA binds to them, they change shape slightly
to allow ions to pass through their central channel. This channel mainly allows negatively
charged chloride ions to enter the neuron to reduce its
excitability. Because of this property of
the GABA channel receptor, GABA is classified as an inhibitory neurotransmitter,
as opposed to excitatory neurotransmitters, such as glutamate which augment the nerve
impulses in the neuron. Glutamate receptors are responsible for the glutamate-mediated
postsynaptic excitatation and are important for neural communication, memory formation,
learning and regulation. GABA is the natural “key” to
the GABA channel receptor’s “lock”. But GABA is not the only molecule that can modify this channel
receptor’s opening. Other molecules can also affect it.
Naurally the Od Force
here withdraws the diversion caused due to inhibition functioned by the GABA
transmitters. Not only that, it makes free from its bondage with the other
molecule or other medication to exclude those to escort the human system in its
said pre-inhibitory stage. Erasing the faulty connection of GABA with the Glutamate receptors it
may back the sufferers the usual neural
communication, memory formation, learning and regulation. Again during the
inhibitory period the GABA’s bondage with neurons causes change of shape
slightly to allow ions to pass through their central channel. The Od Force in question reverses this
process from inward to outward.
At least two distinct classes of GABA receptor, GABAA and GABAB are there. They
differ in their pharmacological, electrophysiological and biochemical
properties. Electrophysiologically the GABAA-receptor complex
mediates an increase in membrane conductance with an equilibrium potential near
the resting level of −70 mV. This conductance increase often is accompanied by
a membrane hyperpolarization, resulting in an increase in the firing threshold
and, consequently, a reduction in the probability of action potential
initiation, causing neuronal inhibition. This reduction in membrane resistance
is accomplished by the GABA-dependent facilitation of Cl− ion influx through a
receptor-associated channel. On the other hand, increased Cl− permeability can depolarize the target
cell under some conditions of high intracellular Cl−. This in turn
potentially can excite the cell to fire or to activate Ca2+ entry via voltage-gated channels and
it may be a physiologically relevant event, especially in embryonic neurons. Electrophysiologically
there remain two GABA-recognition
sites per GABAA-receptor complex. An increase in the concentration
of GABA results in an increase in the mean channel open time due to opening of
doubly liganded receptor forms, which exhibit open states of long duration. The
increase in the ionic permeability of the GABAA receptor complex is transient in the continuing
presence of agonist. This phenomenon is known as desensitization and is rapidly
reversible GABAB receptors are coupled indirectly to K+ channels. When activated, these receptors
can decrease Ca2+ conductance
and inhibit cAMP production via intracellular
mechanisms mediated by G proteins. GABAB receptors can mediate both
postsynaptic and presynaptic inhibition. Presynaptic inhibition may occur as a
result of GABAB receptors
on nerve terminals causing a decrease in the influx of Ca2+, thereby
reducing the release of neurotransmitters.
If the above narrated activities are once established the human
system becomes escorted on a new disease focus shifting from the focus of the
the previous disease as the said establishment comes in addition with the the
already sufferings of the human system as diversion.The said establishment
undergoes a reversed tract travel under the suviellence of the Od Force in
question here to back to the previous condition of the diseased human system
which results the withdrawal of the inhibition.
The complex includes five major binding domains. These include
binding sites localized in or near the Cl− channel for GABA. These binding domains modulate receptor
response to GABA stimulation. All establishments undergo the withdrawl of the
said burdens of the bondages as the said Od Force activates the deactivation/stimulation
caused due to binding. The benzodiazepine
receptor is an integral part of the GABAA receptor—Cl− channel complex. Benzodiazepine
receptor-binding sites copurify with the GABA-binding
sites. The benzodiazepine agonists enhance GABAergic transmission.The frequency
of channel opening in response to GABA
beomes increased. Bonding at the binding sites may act by increasing the
proportion of channels opening to the longest open state while reducing the
proportion opening to the shorter open states resulting in an overall increase
in mean channel open time and Cl− flux.
Channel blockers cause a decrease in mean channel open time working by
preferentially shifting opening channels to the briefest open state. Both
appear to act on the gating process of the GABAA receptor channel, but their effects on
the open states are opposite to each other. An action may cause preventing Cl− channel permeability. The channel
blocker with a net negative charge, blocks the channel by interacting with the
positively charged amino acid residues within the channel pore, consequently occluding
Cl− passage through
the channel. The Od Force lifts all the said blocks and inhibition to normalize
the conditions.
Actually the Od Force in question withdraws the diversion caused
by the enhanced GABA-mediated Cl− conductance.
It finally cancels the strong positive relation that was played chemically to
cause stimulation of GABA-mediated Cl− uptake, amino acids critical sensitivity
in the membrane-spanning domains etc.
Intoxication activities like vomiting, stomach ache,
diarrhea and gastroenteritis follow the absorption disorders, headache, nervous
agitation and chronic convulsions, and symptoms of liver and renal toxicity
extending to yellow liver atrophy, arrhythmia and myocardial bleeding is
withdrawn by this Od Force. This Od Force is highly appreciated in withdrawing
the induced severe metabolic disturbances. Intoxication may be accompanied by
an irritant effect on the gastrointestinal tract, uterus, liver and kidney
which may also be withdrawn in the activities of the Od Force.
The development of immunopharmacological potential over the human
system is highly liftable from its sitting in the human system. It is
highly capable of erasing the inhibited human immunonodeficiency virus
(HIV)-dependent cell death. MT-4 cells remain unaffected. Whereas infected MT-2 cells are under the
control of this Od Force to exhibit the inhibited HIV-1-specific antigen
expression.
It
causes withdrawal of the stimulation to increase in the proliferation rates of
spleen cells. It is highly anti-mitogenic on the peripheral blood leukocytes.It
is easily learnable that caused T-cell induction particularly of the
CD4-positive T-helper/inducer cells in connection with an increased production
of interleukin-2 (IL-2) may be vanquished. The mitogenic and cluster-forming
activity causing T-cell induction particularly of the CD4-positive
T-helper/inducer cells in connection with an increased production of
interleukin-2 (IL-2) may be withdrawalable easily. This indicates that not only
proliferation but also a differentiation to fully functional T-helper cells
taken place is withdrawable by this Od Force. Only T cells, not B cells, come
under the stimulation of this Force. The activation occurrs only in the
presence of the monocyte/macrophage fraction and it comes under the
neutralization by antibodies against interferon (IFN)-γ and IL-1. Induced IFN-γ
production in CD4+ cells
was assumed to be the mode of action, whereby the IFN-γ produced stimulated
monocytes/macrophages to produce IL-1 is also under reversible under this Od
Force. As a second signal of the T-cell activation, this triggeres the
expression of IL-2 receptors and the production of IL-2 in CD4+ T-helper cells. In all these cases
impending actions may be taken back by this Od Force. Any deviation may be
backed by this Od Force.
The increasing secretion of the cytokines IL-1, IL-6 and tumor
necrosis factor-α (TNF-α) is also controlble in this Force. . It is capable of
reversing the reversed process that may increase in the production of IFN αβ.
The Od Force in question causes influence to impose anti-oxidative
measure on the oxidative metabolisms of the macrophases. It causes a decrease
in the number of antibody-producing lymphocytes in the hemolytic plaque assay.
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