Thuja occidentalis

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 Immunostimulant boosting over the immune system to loose the phlegm as an expectorant is withdrawn by this Od Force.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diversion caused further in the tackling or in decreasing the toxic effects of chemotherapy and radiation therapy is withdrawn as this Od Force is administered.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, GABA_A and GABA_B are there. They differ in their pharmacological, electrophysiological and biochemical properties. Electrophysiologically the GABA_A-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 GABA_A-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 GABA_A receptor complex is transient in the continuing presence of agonist. This phenomenon is known as desensitization and is rapidly reversible GABA_B 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. GABA_B receptors can mediate both postsynaptic and presynaptic inhibition. Presynaptic inhibition may occur as a result of GABA_B 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 GABA_A 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 GABA_A 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 α_β. 

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.