Euonymus Europaeus
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Celastraceae
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Tree
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Spindle Tree
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The Od Force of the fruits, seeds and wood of this plant is used
as one of the components in the preparation of remedy. It is poisonous. Though
the poison is present throughout the plant it is the berries which causes harm
mostly.
Symptoms appearing materially or chemically involve diarrhea,
vomiting and stimulation of the heart. The cell to cell negatively charged
electromagnetic pathways circuit(s) becomes profoundly involved in this
deactivation to cast hallucinations, loss of consciousness and sufferings of
meningitis with a strong base on gradual intoxication on the way of more
poisoning. The circuit(s) may be extended to cause kidney failure to end the
sufferings in the circulatory failure. The Od Force in question here accounts
for lifting the material use borne suspension of the Od Force that was
travelling in the deactivated circuit(s). Nausea, dizziness and strong stomach pain
etc. are withdrawn herewith. And in this way death from the poisoning with
chemical cancellation is reversed to life with the reestablished failed
circulatory system.
It withdraws the stimulated appetite and flow of gastric juice. It
is anti-irritant to the intestine and is anti-cathartic. The loss of the Od
Force of the human organism as a result from the material use to cause diuretic
and expectorating functions is met up herewith. The material or chemical shifts
from the material uses of the purgative in case of constipation with liver
disorders particularly followed or accompanied with fever are erased herewith.
It lifts the stimulation from the liver and promoted activities to cause flow
of bile. Fatal blood-stained diarrhea and convulsions which may result death is
also within the withdrawal activities of this Od Force. Paralysis of the
digestive tract and inflammation of the intestines are withdrawn herewith. It
is well in treating the scabies, lice (head, body or pubic), tick and other
skin parasites with the addition of the Od Forces as are lost due to the
activities of those.
This Od Force is similarly an anti-malarial. It cancels the
established stimulation in the nutritive process. The material shifts resulted
from the materially or chemically lifted dropsy caused from the liver and renal
inactivity, are withdrawn herewith.
It exhibits the phosphodiesterase, cyclic
nucleotidephosphodiesterases inhibition. In its activities it decreased the
raised intracellular cAMP,
deactivates the activated PKA, exhibits the inhibited TNF-alpha and leukotriene
synthesis and increased the reduced inflammation and innate immunity and
functions as agonist against adenosine
receptor antagonist.
As a phosphodiesterase
inhibitor, the phosphodiesterase enzymes
are prevented from converting the active cAMP to an inactive form. cAMP
works as a second messenger in many hormone-
and neurotransmitter-controlled metabolic systems, such as
the breakdown of glycogen. When the inactivation of cAMP is inhibited materially, the
effects of the neurotransmitter or hormone that stimulated the production of
cAMP are much longer-lived. In general, the net result is a stimulatory effect.
This Od Force erases the material shifts caused from these stimulatory effects
rewinding the described passage.
It works to lift the vasodilator (a
blood vessel widener) and the heart,
especially myocardial stimulant activities. In treating the high blood pressure
the material’s ability to dilate blood vessels is used. But this is caused at
the cost of further loss of the Od Force from the human system to sum up the
same with the loss as was performed during the establishing the said blood
pressure. So this Od Force erases out the dilation of the blood vessels.
Diversions came from materially treated other circulatory problems including arteriosclerosis,
certain vascular diseases, angina
pectoris etc. might be withdrawn also herewith. The deactivated cell to cell
negatively charged electromagnetic circuit(s) caused by syphilitic angina attacks and degenerative angina are
hereby reactivated to cure the same erasing the diversions received from the
material or chemical treatments of those.
Materially improved
microhardness of tooth enamel which could potentiality increase resistance to
tooth decay is also associated with the loss of the Od Force with a new focus
of disease. This focus can be withdrawn with the administration of this Od
Force. The loosening of the muscles in the bronchus caused helps alleviate the
symptoms of asthma is withdrawn herewith.
It draws the attention of the
torture experienced by the vagus nerve caused by the antitussive or cough
reducing material to lift the same. Similarly the relaxed smooth muscle in
bronchi in treated asthma also experiences the need of this Od Force. The
prostate cancer in older man, prenatal and infant hypospadias and testicular
cancer are targets of this Od Force.
It
vibrates the deactivated cell or cell to cell negatively charged
electromagnetic circuit(s) to cancel the process of inducing to cause genetic
mutation. It has tremendous
constructional effects on the adenine and guanine bases
of deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). It breaks
the reversible blocks against the action of adenosine on its receptor and
consequently withdraws the respective chemical or material diversions or shifts
caused from the onset of drowsiness induced by adenosine. It makes free certain
portions of the autonomic nervous system from established stimulation. The
material or chemical shifts from the materially treated prematured
bronchopulmonary dysplasia and apnea may be used to make week the basement of
the diversion or shift. In cases of such types of shift caused from the Parkinson’s
disease, cardiovascular disease such as coronary artery and stroke are also
subjects of this Od Force to be weakened at their own bases.
It
withdraws the established delay in the onset of muscle fatigue and central
fatigue. It puts its softening effects on the arterial stiffness. Materially affected gastrointestinal motility and
gastric acid secretion are withdrawn herewith. Increased basal metabolic rate
is also lifted herewith. In cases of postmenopausal women established
acceleration in causing bone loss is removed herewith.
Gene polymorphism could be associated with caffeine withdrawal
symptoms and beta-1 and beta-2 play roles in this withdrawal. Compared to people with homozygous Gly16 allele, people with the
heterozygote ADR beta-2 Gly16 Arg gene polymorphism have a higher chance of
feeling fatigue after 48 hours of caffeine withdrawal. Probably beta2-
adrenoceptors are the main cause for this increase in mental fatigue symptoms. Beta
2- adrenoceptors are receptors that regulate glycogenolysis, secret insulin and
intramuscularly transport glucose that is used for cerebral and muscle
activity. The genes ADRbeta1 Gly16 Arg and CYP1A2-163A>C polymorphisms are
associated with peoples' mood swings and increased depression level. Among
subjects homozygous for the CYP1A2 allele, ADRbeta1 Gly389 allele carriers are
reported to have a higher percentage of depression level increase when compared
to Arg389 homozygotes subjects. Adrenergic receptors, again, play a key role in
this symptom, as altered norepinephrine (an adrenoceptor agonist)
neurotransmission contribute to the etiology of depression. This symptom is
often seen in faster caffeine metabolizers, because caffeine effects diminish
quicker in these people and provide them less opportunity to adapt to caffeine
loss. In all cases discussed above here the Od Force in question opposes the
caused loss of the Od Force by reactivating the deactivated cell to cell
negatively charged electromagnetic circuit(s) created by the chemical reactions
between the human cellular system and the applied material.
Again Beta(1)- and beta(2)-adrenoceptors (AR)
play a pivotal role in regulation of the cardiovascular system. Both beta-AR
subtypes are polymorphic. There are two major single nucleotide polymorphisms
(SNPs) in the beta(1)-AR gene: the Ser49Gly and Arg389Gly beta(1)-AR
polymorphisms. In recombinant cell systems Gly49 beta(1)-AR is much more
susceptible to agonist-promoted downregulation than Ser49 beta(1)-AR, while
Arg389 beta(1)-AR is three to four times more responsive to agonist-evoked
stimulation than Gly389 beta(1)-AR. There are three major SNPs in the
beta(2)-AR gene: the Arg16Gly, Gln27Glu and Thr164Ile beta(2)-AR polymorphisms
(occur in humans only in the heterozygous form). In recombinant cell systems
Gly16 beta(2)-AR is much more susceptible to agonist-promoted downregulation
while Glu27 beta(2)-AR is rather resistant to agonist-induced downregulation
but only in combination with Arg16, that occurs naturally extremely rare.
Thr164 beta(2)-AR is three to four times more responsive to agonist-evoked
stimulation than Ile164 beta(2)-AR. This review speaks of the possible
relationship of these polymorphisms to cardiovascular diseases. It is appearing
that the cardiovascular diseases such as hypertension, coronary artery disease
and chronic heart failure, beta(1)- and beta(2)-AR polymorphisms do not play a
role as disease-causing genes; however, they might affect material responses.
Thus, it might be possible, by assessing the beta(1)-AR genotype, to predict
responsiveness to beta(1)-AR agonist and -blocker treatment: patients
homozygous for the Arg389 beta(1)-AR polymorphism should be good responders
while patients homozygous for the Gly389 beta(1)-AR polymorphism should be poor
responders or non-responders. Furthermore, subjects heterozygous for the
Thr164Ile beta(2)-AR polymorphism exhibit blunted responses to beta(2)-AR
stimulation. Finally, the Arg16Gln27 beta(2)-AR haplotype appears to be - at
least in human vascular and bronchial smooth muscles - rather susceptible to
agonist-induced desensitization (in contrast to the recombinant cell system
findings), and might have some predictive value for poor outcome of heart
failure. So in cases of vascular or
muscular diseases here also the applied material is doing the detachment of the
Od Force of the human organism further in the way of causing the chemical
reaction with the human system material for which total loss of the Od Force
expresses itself through some altered focus and the patient gets betterment
from his impinging sufferings. The Od Force in question washes the underlying
chemical or material diversions caused from the materially treated
hepatocellular and endometrial cancer. The shift may be expressed in a
colorectal cancer or bladder cancer and the administration of this force will
salvage the human organisms suffering from this colorectasl cancer to its
previous Od Force situation by activating the deactivated cell to cell
negatively charged electromagnetic circuit(s) which is resulted in course of
the chemistry action of the material given for the treatment of the said hepatocellular
and endometrial cancer etc. It is equally smart to lift the diversions caused
from the materially treated Alzhemer’s disease, type -2 diabetes. Increased
intraocular pressure with glaucoma is withdrawn herewith. The serious
material or chemical shifts from the liver cirrhosis is erased herewith
similarly.
The
undergoing restlessness, fidgeting, anxiety, excitement, insomnia, flushing of
the face, increased urination, gastrointestinal disturbance, muscle twitching,
a rambling flow of thought and speech, irritability, irregular or rapid heartbeat,
and psychomotor agitation, mania, depression, lapses in judgment,
disorientation, delusions, hallucinations, or psychosis, rhabdomyolysis (breakdown
of skeletal muscle tissue) are also the subjects of this Od Force.
Its mechanism of action is as an anti-antagonist
of adenosine receptors in the brain. When a person is awake and alert, little
adenosine is present in (CNS) neurons. With a continued wakeful state,
over time it accumulates in the neuronal synapse in turn binding to and
activating adenosine receptors as are found in certain CNS neurons; when
activated, these receptors produce a cellular response that ultimately
increases drowsiness. Materially an antagonizing effect is fallen on the adenosine
receptors. Adenosine is prevented from activating the receptor by blocking the
location on the receptor where adenosine binds to it. As a result, drowsiness
is prevented, and thus restores alertness is maintained. But it is at the cost
of chemical or material shift. This Od Force is capable of lifting the above
shift(s) or diversion(s).
It functions an anti-receptor antagonist at all
adenosine receptor subtypes (A1, A2A, A2B and A3 receptors). As
an anti-antagonism at these receptors it withdraws the established stimulation
from the medullary vagal, vasomotor, and respiratory centers by decreasing the
increased respiratory rate, lifting the reduced heart rate, and cancelling the
constrictions from the blood vessels. As an adenosine receptor anti-antagonism
also downs the promoted neurotransmitter release (e.g, monoamine and
acetylcholine), adenosine activities as an inhibitory neurotransmitter
that suppresses activity in the central nervous system are reversed herewith. Palpitations
of heart caused by blockade of the adenosine A1 receptor are cancelled here
again by lifting the said blockade.
Material both water- and lipid-soluble crosses the blood-brain
barrier that separates the bloodstream from the interior of the brain.
Once in the brain, the principal mode of action is as a nonselective antagonist
of adenosine receptors, an agent that reduces the effects of adenosine. This Od
Force is capable of losing the binding to adenosine receptors on the surface of
cells acting as a anti-antagonist.
In addition to its activity at adenosine receptors, it functions
as an inositol triphosphate receptor 1anti-antagonist and a voltage-independent
deactivator of the ryanodine receptors (RYR1, RYR2 and RYR3). It is also an anti-antagonist of the
ionotropic glycine receptor.
It indirectly opens bind
to any dopamine receptors. It influences opening of binding of dopamine at
its receptors in the striatum by opening the binding to adenosine receptors that
forms GPCR heteromers with dopamine receptors, specifically the A1—D1 receptor
heterodimer (this is a receptor complex with 1 adenosine A1 receptor
and 1 dopamine D1receptor) and the A2A-D2 receptor heterodimer (this
is a receptor complex with 2 adenosine A2A receptors and 2
dopamine D2 receptors). The A2A–D2 receptor
heterotetramer has been identified to mediate some of its psychostimulant
effects and its pharmacodynamic interactions with dopaminergic psychostimulants.
Materially caused release of dopamine in the dorsal striatum and
nucleus accumbens core (a substructure within the ventral striatum), but
not the nucleus accumbens shell, by anti-antagonizing A1 receptors in the
axon terminal of dopamine neurons and A1-A2A heterodimers (a
receptor complex composed of 1 adenosine A1 receptor and 1
adenosine A2Areceptor) in the axon terminal of glutamate neurons is
withdrawn herewith. It reestablishes the lost material tolerance in the nucleus
accumbens core by lifting the inductive effects over the materially induced
dopamine release.
It acts as exhibitor against the phosphodiesterase
inhibition. As exhibitor it decreases the raised
intracellular cAMP, deactivates the activated protein kinase A, exhibits
the inhibited TNF-alpha and inhibited leukotriene synthesis and lifts the
reduced inflammation and innate immunity. It also affects the cholinergic
system by exhibiting the inhibited enzyme acetylcholinesterase.
It opposes the antagonizing material activities over the
adenosine A2A receptors in the ventrolateral preoptic area (VLPO) withdrawing
the reduced inhibitory GABAneurotransmission to the tubermammillary nucleus, a
histaminergic projection nucleus that activation-dependently promotes arousal.
It imposes its withdrawal activities over the materially caused
mutation on selected chromosomes.
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