Canabis Sativa

Canabis Sativa

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Cannabaceae

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Shrub

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Hemp

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                    The Od Force of the flowering top is used as one of the components in the preparation of the remedy. It is non-poisonous.

                     It reverses the induced psychoactivity of the human system. It is usable in changing the direction along which the diversion caused from the chemical treatments of various ailments such as, asthma, cystitis, diarrhoea, desentry; gonorrhoea, gout, epilepsy, malaria, fevers etc.It is in reality withdraws the diversions caused by the chemicals used as anodyne, anti-inflammatory, antispasmodic, cholagogue, diuretic,emollient,hypnotic, hypotensive, laxative,narcotic,ophthalmic, sedative,  HIV/AIDS, glaucoma, other eye problems, cachexia, pain, muscle spasticity, convulsion, insomnia, depression,Cachexia,Neuralgia, Rheumatism, Hysteria etc. It escorts the already carrying the diversion burdens human system from the dangerously cornered from the further closing of the way to nausea and vomiting by the some new chemical, if it is in its own capacity.It lifts the torture done chemically over the anorexia nervosa to increase food intake. It saves the patients from the sufferings caused by the externally chemical treatment on gout, sores, varicose veins and rheumatism. It sweeps the narcotic intoxication with hallucination, dizziness and dysphoria. It appears to be effective to lift the diversions caused by the chemical treatment of old pain including the pain caused by neuropathy and also that due to fibromyalgia and rheumatoid arthritis. It withdraws the cannabinoid hyperemesis syndrome. Diversions caused from the chemically treated neurological problems including multiple sclerosis, epilepsy and movement problem, spasticity are under the control of this Od Force. Categorically the Od Force in question increases the reduced nausea, drags the stimulated appetite, fights against the diversions caused from the chemically treated depression, chemically treated uplifted cerebral effect, chemically relieved headaches and migrains, relaxed muscles, relieved pain, chemical action for expectoration, Crohn’s and Parkinson’s diseases, Asthma and Emphysema, skin diseases such as pruritis and psoriasis, muscle spasm, paraplegia and quadriplegia, insomnia. It erases the new focus caused from the activity done to cause bronch-dialation chemically. It sweeps the dusts obtained in the form of the further loss of the Od Force of the human system as a result to put chemicals to tackles the type 2 diabetes and related metabolic disorders. It further lifts the burden of the another loss of the Od Force due to chemically treated to cause retardation of the growth of lungs in Lewis lung adenocarconoma

There are two well characterised cannabinoid receptors with distinct physiological properties. The CB1 receptor mediates most of the psychoactive effects of cannabinoids, whereas the CB2 receptor is principally involved in anti-inflammatory and immunosuppressive actions. Without caring for finding for selective CB2 receptor activation to provide potential to the anti-inflammatory effects of cannabinoids without the psychoactive effects the Od Force here itself is capable enough to lift the blockages over the CB1 and CB2 receptors done chemically.It gives back suffering human system reestablishment of the role of CB1 in neuroprotection and neurodegeneration. It perhaps reestablishes the following mechanisms of CB1-mediated neuroprotection-------1. It helps start of the endocannabinoid activation of pre-synaptic CB1 receptors to reduce neurotransmitter release and, hence, excitotoxicity in post-synaptic neurons. 2. To reinvolve the CB1in the regulation of the vasidialation, both directly through vascular CB1 receptors and indirectly through the inhibition of the vasoconstrictor endithelin-1. Thirdly it is through the regulation in the release of proinflammatory factors such as NO and TNF-α in the acute phase of the brain injury.

On the contrary CB2 is believed to be devoid of psychoactivity, and has significant anti-inflammatory functions. Inflammation is known to be a critical part of many types of neurodegeneration. The Od Force hare help the suffering system stop the neurodegeneration.

It lifts the diversion effects of the ‘immunosuppressive’ and ani-inflammatory chemical activities. Both of the CB1 and CB2 receptors have been found mediating the leucocytes for inflammation. But CB2 is widely and strongly engaged in expressing itself in the range of the leucocytes and it is the key mediator of cannabinoid regulation of the inflammation and immune functions.  In this situation the Od Force in question is quite comfortable to establish the derailed regulation of the inflammation and immune functions.

CB2 receptors are implicated in a range of leukocyte functions. Blockage over the CB2 receptor may inhibit splenocyte proliferation and induces apoptosis. CB2 also regulates B and T Cell differentiation, and the balance of T helper (Th1) pro-inflam-matory to Th2 anti-inflammatory cytokines. In macrophages, CB2 stimulation suppresses proliferation and the release of pro-inflammatory factors such as NO, IL-12p40, and TNF-α, inhibits phagocytosis, and reduces IL-2 signalling to T-cells. CB2 activation also suppresses neutrophil migration and differentiation, but induces natural killer cell migration. In order to resue the suffering human system from its deep sunk loss crisis of the total Od Force this Od Force reverses the chemical activities done imposed on the said human system.

The consistency of CB2 receptors in leukocytes with an anti-inflammatory and immuno-suppressive role regulates inflammation in a diverse range to include gastro-intestinal inflammation, acute hindpaw inflammation, and pulmonary inflammation. Naturally any damage/derailment of in the said consistency is quite withdrawable under the functions of this Od Force. A selective partial agonist may have strong anti-inflammatory hyperalgesia effects, ataxia and other CNS effects may not be observed but all of them may be due to activation of the CB1 receptor. Whatever may be the case in reality the Od Force in question is quite smart to lift the diversion caused but the selected. CB2 expression may be described in a select population of vagus nerve cells and ferret brainstem and may be demonstrated through the role of CB2 in the control of emesis which is regulated through these pathways. This may be a special case, as these CB2-positive neurons may be considered as peripheral nerves that enervate the CNS. However, this finding enhances the likely ‘side effect’ profile for CB2-selective agonists. The Od Force is here is quite competent in erasing the ‘side effect’ profile. Moreover many mediators of peripheral inflammation are also involved in neurodegenerative processes, including various growth factors, inflammatory chemokines and cytokines, and nitric oxide.

Microglia are established in the brain early in development, although it also appears that perivascular microglia have a monocyte origin and may replenish the CNS throughout adult life. Resting microglia is not dormant, but carries out a number of metabolic functions, and through a branching set of extended processes continually monitor the CNS environment. Various stimuli can then induce the microglia to assume various phenotypes, depending on the nature and the scale of the stimuli. When fully activated, microglia is amoeboid and phenotypically indistinguishable from macrophages, and carries out the various roles that macrophages perform in the periphery, including pro- and antiinflammatory functions, and antigen presentation to immune cells. Microglia are activated within hours of CNS injury, whereas monocytes and other cells are not able to penetrate the blood brain barrier for up to several days, at which stage blood-borne immune cells complement the microglia in the regulation of inflammation. Because of their early activation and their extensive distribution and numbers, microglia represents a critical step in the development of CNS inflammation. The Od Force may have important role in returning the human system from the diversion done chemically in prior stage.

 Microglia cluster at β-amyloid plaques in Alzheimer’s diseased brains is worthful. . The distribution of reactive microglia correlates with areas of neuronal loss of Alzheimer’s disease, and inflammation is known to be involved in the pathogenic cascade. Chemokines and cytokines produced at plaques are not blood derived, but are produced by local neurons and glia. However, while microglia is involved in the metabolism and clearance of β amyloid, it isn’t known whether microglial reactivity and inflammation is a cause or consequence of β-amyloid accumulation. It is known that in animal models the build up of β-amyloid can be dissociated from neuronal damage by blocking microglial activation and that β-amyloid can induce microglial reactivity. Therefore, it is plausible that reactive microglia is central to the neurodegenerative cascade in Alzheimer’s. For instance, release of TNF-α from microglia can stimulate glutamate release from astrocytes, which may contribute to NMDA-receptor mediated neurotoxicity.

Again microglia and neuroinflammation are central to other chronic neurodegenerative diseases, such as Huntington’s disease and Parkinson’s disease.  This Od Force may withdraw the hang over behind the non-activity that stimulates microglial reactivity, and induces the expression of various pro-inflammatory factors such as IL-1β, IL-6, TNF-α, COX-2, and iNOS. Microglia may be activated in both the substantia nigra and the striatum. This is correlated with a loss of tyrosine hydroxylase expression in the striatum. It is capable of withdrawing the effects of microglial neurotoxicity.

It withdraws the diversions caused from the relieved convulsion, inflammation, anxiety, nausea and inhibited cancer cell growth. It is extremely serious to lift the diversed effects caused in the process of making as effective as atypical antipsychotics in treating schizophrenia chemically. It cancels the sufferings caused from the reduced groth of the aggressive breast cancer cells. This indicates that this Od Force leads to perish the diversion caused from down-regulation of tumor aggressiveness. It works, as if, in opposite direction along which the aneuroprotective antioxidants act. It erases the bad effects that appear from the chemical sedative and analgesic activities. It withdraws the other sufferings caused from the causation of the lowering of intra-ocular pressure. We can not its activity to delete the loss of memory to give back the memory.

Cannabichromene(CBC):
Promotes the effects of THC and has sedative and analgesic effects.

Cannabigerol (CBG):
Has sedative effects and anti-microbial properties as well as lowering intra-ocular pressure. CBG is the biogenetic precursor of all other cannabinoids.

Cannabinol (CBN):
A mildly psychoactive degradation of THC, it's primary effects are as an anti-epileptic, and to lower intra-ocular pressure. 

Cannabidiol (CBD):
A major constituent of medical cannabis. CBD represents up to 40% of extracts of the medical cannabis plant. Cannabidiol relieves convulsion, inflammation, anxiety, nausea, and inhibits cancer cell growth.  Recent studies have shown cannabidiol to be as effective as atypical antipsychotics in treating schizophrenia. In November 2007 it was reported that CBD reduces growth of aggressive human breast cancer cells in vitro and reduces their invasiveness. It thus represents the first non-toxic exogenous agent that can lead to down-regulation of tumor aggressiveness. It is also aneuroprotective antioxidant.  Also lessens the psychoactive effects of THC and has sedative and analgesic effects.

Cannabichromene(CBC):
Promotes the effects of THC and has sedative and analgesic effects.

Cannabigerol (CBG):
Has sedative effects and anti-microbial properties as well as lowering intra-ocular pressure. CBG is the biogenetic precursor of all other cannabinoids.

Cannabinol (CBN):
A mildly psychoactive degradation of THC, it's primary effects are as an anti-epileptic, and to lower intra-ocular pressure.