-----------------
Shrub
--------
Hemp
----------
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.