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Apocynaceae
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Shrub
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Lessar periwinkle
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The Od Force of the whole
plant with roots and fruits is used as one of the components in the preparation
of the remedy. It is non-poisonous chemically.
The Od Force pacifies the
stimulated blood circulation to the brain that has been made to enhance
cognition in patients with dementia and enhance memory and learning in patients
with degenerative and vascular dementia in the brain diseases. Dementia may be
caused due to insufficient blood supply to the brain. The required blood
circulation may be caused chemically but at the cost of further deficiency in
the total already remained fund of the Od Force of the considered human system.
This stimulation will naturally cause a new focus to show that the stimulated
blood circulation has cured the diseases due to insufficient supply of blood
like dementia.
The arteriosclerosis
insufficient blood circulation will also create a new disease in the same way
when that is ‘cured’ chemically in the same way presenting us a more grave new
disease. And this Od Force will also do its best job to erase out the loss of
the Od Force caused in the process of ‘curing’ the arteriosclerosis.
The Od Force in question here
posses such quality energic vibrations that this Od Force salvages the human
system from the fathomless severities of loss of the Od Forces caused by the
chemically treated leukemia, lymphoma and other cancer. It is anti-astringent
and withdraws the focus appeared due to the causation of healing outside the
human physique. It withdraws the diversions caused by the chemically treated
internal bleeding, heavy menstrual bleeding and even nose bleeding, bleeding
haemorrhoids as if vasodilator. It withdraws the antispasmodic activities or
established antispasmodic activities. It adds the hypotensive loss of the Od
Force of the human system.
This
Od Force is a Microtubule-constructive remedy. Different wave parts of this Od
Force put itself differently to make free the Microtubule
from its oppression done chemically during the cytotoxicity activities.
Generally at the zone of low frequency that is, at low dilutions it withdraws
the suppression or oppression done chemically on the Microtubule dynamics. The
higher frequency of the higher dilutions vibrates the deactivated
electromagnetic network field of the suffering human system to construct its microtubule
polymer mass that is, the Od Force in question gradually lifts the imposed reducing
activities that reduce the microtubule polymer mass. The Od Force in question
here also applies itself against the playing activity that produces microtubule
fragments by stimulating microtubule minus-end detachment from their organizing
centers. The Od Force here cancels further the performances of enhancing
microtubule detachment from spindle poles correlated best with cytotoxicity.
The
spindle is a dynamic self-assembling machine that coordinates mitosis. The
spindle’s function depends on its ability to organize microtubules into poles
and maintain pole structure despite mechanical challenges and component
turnover. It withdraws that force which disorganizes the activity that rapidly
and robustly pulls severed microtubules and chromosomes poleward overpowering
opposing forces and regaining the spindle architecture. The cytotoxicity imposes
this disorganizing activity if it is in its capacity. It helps the NuMA and dynein/dynactin to regain their mediating duty towards the
pole formation. Transport is powered by dynein pulling on the minus
ends of severed microtubules. NuMA and
dynein/dynactin are specifically enriched at new minus ends within seconds
reanchoring minus ends to the spindle and delivering them to poles. This force
on minus ends represents a newly uncovered chromosome transport mechanism that
is independent of plus end forces at kinetochores and is well suited to
robustly maintain the spindle mechanical integrity. The chemical reactions
caused during the period of the cytotoxicity makes minus of that Od Force which
organizes the above functions. And naturally the said Od Force escorts the
deficient human system in the land of the plus of that Od Force that had been
robbed during the time of the cytotoxicity.
Microtubules are required for the establishment of cell
polarity, polarized migration of
cells, intracellular vesicle transport, and chromosomal segregation in mitosis. Microtubules (MTs) are non-equilibrium
polymers of α/β-tubulin heterodimers, in which GTP hydrolysis on the β-tubulin
subunit occurs following assembly. Most microtubules are nucleated from
organizing centers. The most prevalent microtubule behavior is dynamic
instability, a process of slow plus end growth coupled with rapid
depolymerization (“catastrophe”) and subsequent rescue. Although microtubule
minus ends show dynamic instability, albeit at a lower rate than the plus ends show dynamic
instability, the minus ends are usually capped and anchored at MT organizing
centers and thus often do not participate in microtubule dynamics.
Maintaining a balance between dynamically unstable and stable
microtubules is regulated in large part by proteins that bind either tubulin
dimers or assembled microtubules. Proteins that bind tubulin dimers include
stathmin, which sequesters tubulin and enhances MT dynamics by increasing
catastrophe frequency, and collapsin response mediator protein (CRMP2), which
increases MT growth
rate by promoting addition
of tubulin dimers onto microtubule plus ends. Other proteins that associate
with assembled MTs include those that bundle MTs (e.g. MAP1c), those that
stabilize MTs (e.g. tau), and those that maintain MTs in a dynamic state
(MAP1b). A major signaling pathway that regulates MT dynamics involves GSK-3β,
a kinase typically active under basal growth conditions but locally inactive in
response to signals that enhance MT growth and dynamics.
In addition to the above factors, many MT motor proteins, and
even non-motor proteins, aid in the dynamics of MTs. Proteins such as Xenopus microtubule
associated protein 215
(XMAP215), promote MT assembly through binding to tubulin dimer to facilitate
its incorporation in the growing plus end. XMAP215 also may compete with some
of the MT plus end binding proteins (+TIPS), of which the end binding protein
EB1 appears to be the master organizer. Complexes between the adenomateous
polyposis coli (APC) protein and plus end binding proteins stabilize MTs by
increasing the duration of the MT elongation phase. MT instability is promoted
by several nonmotile kinesins from the kinesin-13 family. The mitotic
centromere associated kinesin, MCAK, one of the most studied kinesin-13 family
proteins, binds both plus and minus MT ends in vitro. The binding of MCAK to a
MT end is thought to accelerate the transition to catastrophe by weakening the
lateral interactions between the protofilaments
Tubulin undergoes several post-translational modifications such
as acetylation, polyglutamylation, and poly-glycylation, which have been shown
to alter the association with certain MT motors as well as other proteins that
can affect MT stability and dynamics.
When the concerned
cytotoxicity causes the chemical reactions between the Microtubules and the chemical
employed depending upon the situation the total phase may be affected
selectively. Whatever be the dilution, whatever the part of the total reaction
as stated above be affected during the establishing period of the cytotoxicity the
concerned Od Force reverses the same to salvage the human system from the lacks
of the Od Force as became recorded in the gene to its previous state.
Cancerous tumors are characterized by cell
division, which is no longer controlled as it is in normal tissue.
"Normal
The ability of chemotherapy to kill cancer
cells depends on its ability to halt cell division. Usually, the drugs
work by damaging the RNA or DNA that tells the cell how to copy itself in
division. If the cells are unable to divide, they die. The faster
the cells are dividing, the more likely it is that chemotherapy will kill the
cells, causing the tumor to shrink. They also induce cell suicide
(self-death or apoptosis).
Chemotherapy drugs that affect cells only
when they are dividing are called cell-cycle specific. Chemotherapy drugs
that affect cells when they are at rest are called cell-cycle
non-specific. The scheduling of chemotherapy is set based on the type of
cells, rate at which they divide, and the time at which a given drug is likely
to be effective. This is why chemotherapy is typically given in cycles.
Chemotherapy is most effective at killing
cells that are rapidly dividing. Unfortunately, chemotherapy does not
know the difference between the cancerous cells and the normal cells. The
"normal" cells will grow back and be healthy but in the meantime,
side effects occur. The "normal" cells most commonly affected
by chemotherapy are the blood cells, the cells in the mouth, stomach and bowel,
and the hair follicles; resulting in low blood counts, mouth sores, nausea,
diarrhea, and/or hair loss. Different drugs may affect different parts of
the body.
transport is powered by dynein pulling on minus ends of severed
microtubules. NuMA and dynein/dynactin are specifically enriched at new minus
ends within seconds, reanchoring minus ends to the spindle and delivering them
to poles. This force on minus ends represents a newly uncovered chromosome
transport mechanism that is independent of plus end forces at kinetochores and
is well suited to robustly maintain spindle mechanical integrity.
The spindle is a dynamic self-assembling machine that
coordinates mitosis. The spindle’s function depends on its ability to organize
microtubules into poles and maintain pole structure despite mechanical
challenges and component turnover. Although we know that dynein and NuMA
mediate pole formation, our understanding of the forces dynamically maintaining
poles is limited: we do not know where and how quickly they act or their
strength and structural impact. Using laser ablation to cut spindle
microtubules, we identify a force that rapidly and robustly pulls severed
microtubules and chromosomes poleward, overpowering opposing forces and
repairing spindle architecture. Molecular imaging and biophysical analysis
suggest that transport is powered by dynein pulling on minus ends of severed
microtubules. NuMA and dynein/dynactin are specifically enriched at new minus
ends within seconds, reanchoring minus ends to the spindle and delivering them
to poles. This force on minus ends represents a newly uncovered chromosome
transport mechanism that is independent of plus end forces at kinetochores and
is well suited to robustly maintain spindle mechanical integrity.
Microtubules are required for the establishment of cell
polarity, polarized migration of
cells, intracellular vesicle transport, and chromosomal segregation in mitosis. Microtubules (MTs) are non-equilibrium
polymers of α/β-tubulin heterodimers, in which GTP hydrolysis on the β-tubulin
subunit occurs following assembly. Most microtubules are nucleated from
organizing centers. The most prevalent microtubule behavior is dynamic
instability, a process of slow plus end growth coupled with rapid
depolymerization (“catastrophe”) and subsequent rescue. Although microtubule
minus ends show dynamic instability, albeit at a lower rate than the plus ends show dynamic
instability, the minus ends are usually capped and anchored at MT organizing
centers and thus often do not participate in microtubule dynamics.
Maintaining a balance between dynamically unstable and stable
microtubules is regulated in large part by proteins that bind either tubulin
dimers or assembled microtubules. Proteins that bind tubulin dimers include
stathmin, which sequesters tubulin and enhances MT dynamics by increasing
catastrophe frequency, and collapsin response mediator protein (CRMP2), which
increases MT growth
rate by promoting addition
of tubulin dimers onto microtubule plus ends. Other proteins that associate
with assembled MTs include those that bundle MTs (e.g. MAP1c), those that
stabilize MTs (e.g. tau), and those that maintain MTs in a dynamic state
(MAP1b). A major signaling pathway that regulates MT dynamics involves GSK-3β,
a kinase typically active under basal growth conditions but locally inactive in
response to signals that enhance MT growth and dynamics.
In addition to the above factors, many MT motor proteins, and
even non-motor proteins, aid in the dynamics of MTs. Proteins such as Xenopus microtubule
associated protein 215
(XMAP215), promote MT assembly through binding to tubulin dimer to facilitate
its incorporation in the growing plus end. XMAP215 also may compete with some
of the MT plus end binding proteins (+TIPS), of which the end binding protein
EB1 appears to be the master organizer. Complexes between the adenomateous
polyposis coli (APC) protein and plus end binding proteins stabilize MTs by
increasing the duration of the MT elongation phase. MT instability is promoted
by several nonmotile kinesins from the kinesin-13 family. The mitotic
centromere associated kinesin, MCAK, one of the most studied kinesin-13 family
proteins, binds both plus and minus MT ends in vitro. The binding of MCAK to a
MT end is thought to accelerate the transition to catastrophe by weakening the
lateral interactions between the protofilaments
Tubulin undergoes several post-translational modifications such
as acetylation, polyglutamylation, and poly-glycylation, which have been shown
to alter the association with certain MT motors as well as other proteins that
can affect MT stability and dynamics.
The spindle is a dynamic self-assembling machine that
coordinates mitosis. The spindle’s function depends on its ability to organize
microtubules into poles and maintain pole structure despite mechanical
challenges and component turnover. Although we know that dynein and NuMA
mediate pole formation, our understanding of the forces dynamically maintaining
poles is limited: we do not know where and how quickly they act or their
strength and structural impact. Using laser ablation to cut spindle
microtubules, we identify a force that rapidly and robustly pulls severed
microtubules and chromosomes poleward, overpowering opposing forces and
repairing spindle architecture. Molecular imaging and biophysical analysis
suggest that transport is powered by dynein pulling on minus ends of severed
microtubules. NuMA and dynein/dynactin are specifically enriched at new minus
ends within seconds, reanchoring minus ends to the spindle and delivering them
to poles. This force on minus ends represents a newly uncovered chromosome
transport mechanism that is independent of plus end forces at kinetochores and
is well suited to robustly maintain spindle mechanical integrity.
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