--------------------------
Droseraceae
---------------
Herb
-----
Sun dew
--------------
The Od Force of
the whole fresh plant is used as one of the components in the preparation of
the remedy.
The diversions
obtained as result of chemical/material and all other dequantization treatment
over various breathing
problems including bronchitis,asthma, whooping cough (pertussis), windpipe infections
(tracheitis), coughing fits, and dry cough
are withdrawn herewith. It escorts the pettorale system from the den of serious
problems of its own. It also takes over the diversion that expresses itself in
the pettorale system as a chemical or material etc. truancy from stomach ulcers
and cancers. It gives back the Od Force in the suffering human system that had
been robbed off from the human system during the dealing of the breaking up the
chest congestion by thinning mucus and making it easier to cough up and
reducing spasm. Generally a deep, violent, spasmodic cough especially whooping
cough associated with increased retching, vomiting, cold sweat and nosebleeds
based diversions are the targets of this Od Force.
Asthma is a chronic disorder in which the
smooth muscles of the bronchial tubes, or air passages, become narrowed,
inflamed and filled with mucus, causing difficulty in breathing. Asthma attack
can be triggered by many irritants, including air pollution, allergens, cold
air and stress. Chemical bronchodilators for emergency relief and inhaled
corticosteroids for long-term in the name of controlling asthma change the
focus of asthma in new disease(s) as because this material reaction takes away
more Od Force from the human system in causing unpleasant new different
sufferings by diverting the immune system of the body to cause relief from
inflammation, relax muscle to reduce the mucus. It is the Od Force as the human
system requires to escorts the human system from the relaxed involuntary
muscles of the respiratory tract, misguided breathing troubles or tightness in
the throat or chest, chest pain, skin hives, rash or itchy or swollen skin. It
salvages the hypoglycaemic human system. It lifts the human system from its
diversion or denned incipient phthisis materially or by some other energy
methods. The shift from the warts and corns caused by the protein digesting
enzymes is also withdrawn. It erases the chemical diversion caused by broken
down resistance of tubercle. It vacates the impending diversion load done
chemically on the M3 muscarinic
receptors in smooth muscle
during the process of causing antispasmodic effects. It
cancels the antiangiogenic effects.
It puts its ability to withdraw the diversions caused by the chemical
exertions of anticancer effects through the concerning antiproliferative and
pro-apoptotic action as well as effects on subcellular signalling pathways. It
significantly puts its activity to withdraw the diversion caused by chemically
reduced proliferation and induced apoptosis of human osteogenic sarcoma (HOS)
cells to lift the chromosomal DNA degradation and apoptopic body appearance,
increase in hypodiploid DNA content and nuclear fragmentation. It erases the
stimulated apoptosis and exhibits the completely inhibited proliferation of the
human pancreatic adenocarcinoma cell lines MIA PaCa-2 and PANC-1. This Od Force
accomplishes these effects by increasing nuclear factor-kappa-B (NF-κB) activity, thereby deactivating the activated
the mitochondrial death pathway which associates the gain of lost mitochondrial
membrane potential (Δψm), cytochrome C gain, and
caspase-3 deactivation. It also offs the diversions obtained as a result of
chemically triggered apoptosis and inhibited proliferation of the human
pancreatic cancer cell lines HPAF-II cells. It elicits similar effects on
chemically diverted pancreatic stellate cells, the progenitors of pancreatic
cancer demoplasia. This exhibitory effects are not only associated with the
unfolding of the suppression of the cell proliferation, deactivating of the
activated caspase-3 but also of withdrawing the induction of poly (ADP-ribosyl)
polymerase cleavage. This Od Force also exhibits the inhibited expression of
Bcl-2, cyclin D1, CDK2, and CDK6 and reversed the induced expression of the
pro-apoptotic protein Bax in tumor tissues. It also exhibits the inhibited
proliferation of ovarian carcinoma ES-2 and PA-1 cells by lifting the arrests
of both cell lines at the G1 phase. It can accomplish these
effects by decreasing the expression of p53 and Cip1/p21 and increasing the expression
of cyclins D1 and E. It can also lift the induced caspase-3-mediated apoptosis
by decreasing the Bax/Bcl-2 ratio, cancelling the chemical diversions caused by
the chemically regulated apoptosis and restored anoikis in both cell lines.
To lift the chemical diversion caused over the
nasopharyngeal carcinoma cell line (NPC-BMI) and apoptotic DNA fragmentation
and increased caspase-3 activity associated with Bcl-2 downregulation with a
view of withdrawing the force that played to reduce the cell viability, it
plays an important role. Furthermore, it exhibits the inhibited human
telomerase reversed transcriptase and human telomerase-associated protein 1,
thereby increasing telomerase activity.
The Od Force also rewinds the molecular mechanisms
involved in chemically induced apoptosis in prostate cancer cells. It cancels
produced antiproliferative effects by exhibiting the inhibited activation of
mammalian target of chemical characterized primarily by its ability to
suppress the immune system, which led to its use in the prevention of transplant rejection and increasing the reduced
intracellular levels of β-catenin in the LNCaP human prostatic cancer cell
line. It also decreases the increased percentage of apoptotic cells by
reversing the downregulated anti-apoptotic proteins and noising the silencing
information regulator 1, human antigen R, and heme oxygenase-1. Furthermore, it
also puts its anti-modulating activities on the modulated expression of
apoptosis-inducing factor and the activation of caspase-3. Finally, it
decreases the increased the expression of the tumor suppressor protein p21. The
protein kinase C (PKC) signaling pathway is critical to cell proliferation, and
over activation leads to abnormal tumor growth.
It cancels the anti-carcinogenic activities to escort the human system
from the chemical diversion. It acts to reverse the downregulating PKC, NF-κB,
and c-Myc while upregulating transforming growth factor-β1 (TGF-β1). The
changed focus due to chemically or materially done Lymphoma prevention
supported by the decrease in cell proliferation, cell viability etc. is
cancelled herewith. It erases the activities that shifts the focus of the
disease due to chemically or materially induced cancer cell death by unblocking
energy metabolism.
In Breast cancer two receptor pathways, estrogen
receptor and tyrosine kinase receptors, especially the epidermal growth factor
receptor family, are drivers of cell proliferation. These pathways are crucial
to the development of both primary and recurrent breast cancers. This Od Force
not only intervenes in the matter of the chemical or material interacts with
and altered effects of these pathways thereby but also lifts the induced cell
death (apoptosis and autophagy) by reversing the influenced kinase signalling.
Furthermore, it withdraws these pathways prevention activities over the mammary
tumors by releasing the suppressed levels of E2-metabolizing enzymes that
occurs during the early-phase E2 carcinogenesi.
Oxidative stress causes genetic instabilities and
functions in the initiation of human cancer. Therefore, effective chemical
inhibition of endogenous oxidative DNA damage measure is taken without knowing
that chemical diversion is caused by this inhibition. This Od
Force has an high effectiveness in cancelling the prevented oxidative DNA
damage to lift the said diversion as reductive.
This Od Force is a naturally occurring broad
spectrum oxidant. The primary antioxidant mechanism chemically attributes to
the direct scavenging of free radicals, nitrogen reactive species, and ROS,
including hydroxyl radicals, peroxyl radicals, NO2 radicals,
and peroxynitrite. Other potential protective mechanisms including the
shielding of DNA from attack and subsequent mutation by its direct association
with this macromolecule, inhibition of ROS production, and chelation of metal
ions, such as copper are caused at the cost of the more serious diversion to
appear as a new focus due to addition of the further loss of the Od Force
together with the loss of the Od Force for which the previous disease had been
caused. This spectacular oxidants salvages the human system from the said
serious now focus.
This Od Force exhibits the
chemical inhibition that we put to prevent the said chemical mediated
oxidatively generated DNA damage. The diversion resulted from the chemical
radical scavenged in the material treatment of the lung fibroblast (V79-4)
cells is also withdrawn herewith. It exhibits the inhibited lipid peroxidation. The significant established increase of the
activities of the antioxidant enzymes superoxide dismutase, catalase, and
glutathione peroxidase in chemical treatment of the V79-4 cell is also cancelled
herewith. In giving the service to withdraw the diversions occurred from the cytotoxic
and antiproliferative activities of chemical/material against cancer cells it
does not affect the normal cell viability generally. Selectively it is anti-cytotoxic
to carcinoma cells but not to normal cells. It is significantly oxidant to lift
the chemical diversions but due to external waste matter expelling and
dependent allied apparatus it may play like some very negligible role of
anti-oxidant. It reverses the modulation in several modulated genes. It
intervenes in the overexpressed genes involved in DNA repair, such as xeroderma
pigmentosum group A complementing protein, DNA ligase III, and DNA excision
repair protein to cause a rewinding effect. By contrast, it reverses the
activity that downregulates mitogen-activated protein kinase and MAP kinase
kinase, which are involved in key cell-signalling pathways. It exhibits the
established chemopreventive inhibition of carcinogen bioactivation,
carcinogen-to-DNA binding, and cancer cell growth.
Tumor metastasis is a
complex cascade that is accompanied by various physiological alterations
involved in angiogenesis, matrix metalloproteinase (MMP) upregulation, and
extracellular matrix degradation; tumor metastasis allows cancer cells to
proliferate and invade blood or lymphatic system, thereby enhancing cancer cell
invasion and worsening prognosis. Actually this complex cascade is associated
with the causation of a complex loosing of the Od Force to leave a complex cell
to cell negatively charged electromagnetic pathways circuits deactivated. Any
chemical prognosis in this situation makes the suffering human system more
distressed causing further loss of the remaining fund of the said human system
with a vague cure.
Angiogenesis is critical to
tumor progression and metastasis .Any anti-angiogenic chemical measure affects
more virulently the suffering human system where angiogenesis itself is a focus
of the some chemically perished focus.
It throws challenge against the diversions caused
from anti-angiogenetic chemical effects that were caused via the VEGFR-2
signaling pathway in breast cancer. The structure-based interaction between the
required chemical used and VEGFR-2 may be analysed. The formed hydrogen bonds
and aromatic interactions within the ATP-binding region of the VEGFR-2 kinase
unit and thus significantly inhibited the series of VEGF-induced angiogenesis
processes, including proliferation, migration, and tube formation of
endothelial cells are reversed to be exhibited.
It demonstrates angiogenic effects by exhibiting MMP-2
activity and secretion, as well as putting it activity against the suppressing
process incurred on the tube formation and migration of vascular endothelial
cells to rewind the same. Suppressed reversion-inducing cysteine-rich protein
with Kazal motifs (RECK) expression in human tumors, including colorectal,
breast, pancreas, gastric, hepatocellular, prostate, and non-small cell lung
carcinoma is reversed herewith. The key action of RECK that has downregulated
MMP-2 activity is withdrawn. Chemically induced RECK at both mRNA and protein
levels associates with the decrease in MMP-2 secretion is lifted herewith.
The inhibition of the expression of the markers of angiogenesis (COX-2,
HIF1α, VEGF, VEGFR, IL-6, and IL-8) and metastasis (MMP-2 and MMP-9) in tumor
tissues is exhibited. In addition, it can significantly exhibit the inhibited
phospho-Akt, Gli1, Gli2, Notch1, Notch3, and Hey1.The reversed
epithelial-to-mesenchymal transition by upregulating E-cadherin and
downregulating Snail, MMP-2, and MMP-9 is also reversed. It can exhibit inhibited pancreatic cancer
growth, angiogenesis, and metastasis by suppressing the Akt, Shh, and Notch
pathways.
It withdraws anti-invasive effects on
androgen-independent human (PC-3) prostate cancer cell lines; it also increases
the decreased secretion of MMP-2 from both cells. The authors further verified
that EA significantly tries to lift the reduced proteolytic activity of
collagenase/gelatinase secreted from the PLS-10 cell line. In addition, it
exhibits the dependently inhibited collagenase IV activity. It can exhibit the
inhibited chemotaxis of the breast cancer cells to stromal cell-derived factor
1α (SDF1α), a chemokine that attracts breast cancer cells to the bone. It can
rewind the inhibited growth of hormone-dependent and hormone-refractory
prostate cancer cells and reverse the processed activity to inhibit on their
migration and their chemotaxis toward SDF1α. Moreover, it can decrease the increased
expression of cell adhesion genes and increase the decreased expression of
genes involved in cell cycle control and cell migration. Furthermore, it can
decrease the increased several well-known tumor-suppression miRNAs, It can
increase the decreased several oncogenic miRNAs, and rewind the inhibited
chemokines receptor type 4/SDF1α chemotaxis axis. The capability of its
exhibitory activity against the inhibition of the invasion of breast and prostate
cancer cells makes this Od Force a potent and effective may function as cancer
prevention.
The protein kinase C (PKC) signaling pathway is
critical to cell proliferation, and over activation leads to abnormal tumor
growth. It acts by reversing the downregulation on PKC, NF-κB, and c-Myc while
downregulating the transforming growth factor-β1 (TGF-β1) to dismiss the chemical
diversion issued to cause prevention. Lymphoma prevention happened by this Od
Force causes the decrease of the increased cell proliferation, cell viability,
and ascite fluid accumulation. The induced cancer cell death by blocking energy
is withdrawable by this Od Force.
Breast cancer is the most commonly diagnosed cancer
among women worldwide. Two receptor pathways, estrogen receptor and tyrosine
kinase receptors, especially the epidermal growth factor receptor family, are
drivers of cell proliferation. These pathways are crucial to the development of
both primary and recurrent breast cancers. It not only interacts with and
rewinds the affection caused on these pathways but also puts withdrawal
activity to reverse the induced cell death (apoptosis and autophagy) by
influenced kinase signalling. Furthermore, these pathways may prevent mammary
tumors by suppressing the levels of E2-metabolizing enzymes during early-phase
E2 carcinogenesis. Diversions caused by the chemically prevented mammary tumors
using these pathways through the suppression of the levels of E2-metabolizing
enzymes during early-phase E2 carcinogenesis are also withdrawn herewith.
It issues directions over the chemical diversions
caused as antiproliferative effects to exhibit the inhibited activation of
mammalian target of certain chemical and to increase the reduced intracellular
levels of β-catenin in the LNCaP human prostatic cancer cell line. It also decreases
the increased percentage of apoptotic cells by upregulating downregulated
anti-apoptotic proteins and sounding the chemically issued silencing
information regulator 1, human antigen R, and heme oxygenase-1. Furthermore, it
rewinds the modulated expression of apoptosis-inducing factor and the deactivating
the activation of caspase-3. Finally, it decreases the increased expression of
the tumor suppressor protein p21.
Acute inflammation is a part of the defence
response, whereas chronic inflammation can lead to hepatocellular carcinoma
(HCC), prostate cancer, colon cancer, breast cancer, and other common forms of
cancer. The link between inflammation and cancer is tight. HCC is an
inflammation-related cancer because the chronic inflammatory state is necessary for the initiation
and development of liver cancer. Several studies have shown that chronic
infections with hepatitis B virus (HBV) and hepatitis C virus (HCV) are major
risk factors for HCC development. Chronic inflammation also affects many
cellular pathways, leading to fibrosis and cirrhosis and finally
hepatocarcinogenesis. Colon cancer is another clear example of the tight link
between inflammation and cancer. Inflammatory bowel disease ranks among the top
three high-risk conditions for colon cancer. The risk for colorectal cancer
increases with the duration and extent of the disease, confirming the active
function of inflammation in cancer development. The regular use of nonsteroidal
anti-inflammatory drugs also lowers the mortality from sporadic colon cancer
and results in the regression of adenomas in familial adenomatous polyposis
patients.
Several pro-inflammatory gene products are crucial
in suppressing apoptosis, proliferation, angiogenesis, invasion, and
metastasis. Among these gene products are TNF and members of its super family,
including IL-1α, IL-1β, IL-6, IL-8, IL-18, chemokines, MMP-9, VEGF, COX-2, and
5-LOX. The expression levels these genes are principally regulated by the
transcription factor NF-κB. NF-κB mediates innate and adaptive immunity by
initiating an inflammatory response to pro-inflammatory signals. NF-κB is
constitutively active in most tumors and is induced by carcinogens, tumor promoters,
carcinogenic viral proteins (HIV-tat, HIV-nef, HIV-vpr, KHSV, EBV-LMP1,
HTLV1-tax, HPV, HCV, and HBV), chemotherapeutic agents, and gamma-irradiation.
The persistent activation of NF-κB in tumor cells alters their ability to grow
and differentiate. One of the best studied consequences of NF-κB activation is
the enhanced survival of cancer cells. The role of persistent inflammation in
aiding tumor development has led to the NF-κB family of transcription factors
being strongly implicated in promoting cancer. Anti-inflammatory agents that
suppress NF-κB or NF-κB-regulated products should have a potential in the
prevention and treatment of cancer.
It possesses
a quality to withdraw the diversions caused by the anti-inflammatory material
or chemicals. It cancels the significant binding affinity with the Rel homology
domain of the NF-κB precursor protein p105 with a binding energy of −7.99 Kcal
and exhibits the inhibited constant of 1.38 μM. It lifts the diversions
resulted from the chemically increased breast cancer cell adhesion and increases
the decreased cancer cell migration. Pro-inflammatory cytokines/chemokines
reduced chemically is also withdrawn herewith.The potentiality of it erases the
chemical shift caused from the decrease of inflammation and inhibition of
cancer progression. This Force withdraws the demonstrated anti-inflammatory
property by downregulating inducible nitric oxide synthase, COX-2, TNF-α, and
IL-6 through the inhibition of NF-κB, which is a prompter of tumorigenesis to
escort the human system prior to this inflammatory stage. It exerts anti-chemopreventive effects on
colon carcinogenesis. It rewinds the reduced TGF-β and IL-6 levels in the LNCaP
human prostatic cancer cells.
It rewinds
the chemical shift obtained from the interacted synergistically in the
induction of apoptosis in the human leukemia cell line, MOLT-4. ROS can selectively and efficiently modifies proteins, thereby,
regulating cellular signaling. When a chemical/material generates ROS. By such
ROS generation the chemical inhibits the activity of topoisomerase-II, which is
achieved through stabilization of topoisomerase-II-DNA cleavable complex in
HL-60 cells. It
May be observed
that the reduced topoisomerase-II activity is linked with reduced level of DNA damage.
The chemically induced generation of ROS induces DNA damage indirectly through
the essential involvement of topoisomerase-II. In this way we may induce
mammalian topoisomerase II-mediated DNA cleavage. Elevation of temperature leads
to a significant reduction in DNA cleavage. The formation of a cleavable
complex steps in topoisomerase II-mediated DNA cleavage induced.
In case of promyelocytic
leukemia cells (NB4), the diversion caused from the causation of generation of
ROS chemically mediated to induced apoptosis is also withdrawn herewith. The
therapeutic diversions of myeloid leukemia are also under the notice of this Od
Force. The inhibition of proliferation of NB4 cells, the morphologically
changed characteristic of cell apoptosis, such as chromosome condensation and
apoptotic body formation, NB4 cells blocking in G2/M phase of cell cycle and
induce apoptosis of APL cell line NB4 cells, caused S-G(2)/M phase arrest and
induced cell death in MEF cells, irrespective of DNA polymerase status are
withdrawn herewith.
The chemical effects
on liver cancer HepG2 cells, inhibition of the migration and invasion of liver
cancer cells through downregulation of MMP-2 and uPA, inhibition of histone
acetyltransferase activity and p300-mediated acetylation of p53.
In performing the
exhibition of such inhibited p300 histone acetyltransferase activity this Od
Force withdraws the potential influence occurred on a number of different genes
that play crucial role in many diseases, including cancer. It erases the
engraved cytotoxic diversions of HEPA-3B hepatoma cell line.
In renal cancer human
embryonic kidney 293 (HEK293) and brain tumor LN229 cells express mainly Nox-4,
a renal NAD(P)H oxidase. It affects the chemical diversions had from the Nox-4
activity in HEK293.
In ovarian cancer
chemically inhibited cell growth in relation to BRCA1 (early onset) status in ER-positive
ovarian cancer cells is exhibited herewith. Induced apoptosis is reversed
through the rewinding process of chemical binding to and modulation of ER in
BRCA1-silenced cells. In Myeloma the
activation of signal transducers and activators of transcription-3 (STAT-3)
that influences carcinogenesis is withdrawn herewith. The inhibited
constitutive and interleukin (IL)-6-inducible STAT-3 phosphorylation and
overexpression of constitutively active STAT-3 that effectively inhibits the apoptosis
are withdrawn. It demonstrates its efficacy in erasing the chemical shift also
in cases of skin carcinomas. It cancels the anticancer affects caused by the
chemicals on melanoma cells. In A375.S2 cells, the Od Force in question is
found to lift the induced apoptosis and S-G2/M cell cycle arrest leading to
inhibition of cell growth inhibition. The elevated level of p21 and reduced
levels of cyclin B1, cyclin A, Cdc2, and Cdc25C are reversed herewith. It also
cancels induction that causes change in Bax/ Bcl-2 ratios and activation of
caspase-9 resulting in apoptotic cell death.
There is a
positive correlation between vitamin K intake and osteoporosis. If this
relation is made negative chemically this Od Force takes an important role to
cancel the negativity done. Diversions caused by the chemical contribution to
weaker bones and increased fractures is swept herewith. It may play a crucial
role in cardiovascular health disturbance. It may be is needed for withdrawing
the diversions caused from the activating protein matrix Gla-protein to reverse
the established chemical activity of inhibiting the vascular calcification. It
erases the chemical shift obtained in the process of preventing the calcium
build up in blood vessels that assist in vascular disease.
The diversion
as discussed above naturally find the focus in the Pettorale system. And
naturally to lift or withdraw this Od Force is called for.
No comments:
Post a Comment