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Stuff & Stuff
Sci-Tech News & Olds
Ultra-censored XXXX-Edition -- Beyond Porn to Tantra !
[August 32, 2018 ]
Contents
Frederick Tombe : Maxwell's
Original Equations
Jeff Rothschild loves you
Barrie Trower :
WiFi : A Thalidomiode in the Making. Who Cares ?
Zhe Liu, et al. : ZL-105 vs Cancer
Cancer Apoptosis by CD95
Magnesium Chloride Potentiation
of Solar Cells
Martin Pohlman : Time
Machine ( US2006073976 : Method of
gravity distortion and time displacement )
John Lilly : Balanced Pulse-Pair
Waveform [ The "Lilly Wave ' ]
10 Search Engines for
Exploring of the Deep / Invisible Web
Fasting vs Cancer
Scientists say nerves use
sound, not electricity
Antoine PRIORE :
Healing of the Acute and Chronic Experimental
Trypanosomiasis by the Combined Action of Magnetic Fields
and Electromagnetic Waves
[ PDF ]
See also : PRIORE : Electromagnetic Therapy
The General Science Journal
Frederick Tombe :
Maxwell's Original Equations
[ PDF ]
Jeff Rothschild love your worthless pseudo-life / existence as
a useless eater-idiot-dupe-slave :
Barrie Trower :
WiFi : A Thalidomide in the Making. Who Cares ?
[ PDF ]
Cancer News -- More High-Tech Pseudo-Hope :
Zhe Liu, et al. : ZL-105
www.sciencedaily.com/releases/2014/03/140325102705.htm
http://www2.warwick.ac.uk/newsandevents/pressreleases/new_drug_raises/
New drug raises potential for cancer
treatment revolution
by
Peter Sadler
A revolution in cancer treatment could soon be underway following
a breakthrough that may lead to a dramatic improvement in cancer
survival rates.
A new study at the University of Warwick, published today in the
journal Angewandte Chemie International Edition, has developed a
new drug that can manipulate the body’s natural signalling and
energy systems, allowing the body to attack and shut down
cancerous cells.
Called ZL105, the drug is a compound based on the precious metal
iridium. The study has found ZL105 could potentially replace
currently used anticancer drugs, which become less effective over
time, cause a wide-range of side-effects and damage healthy cells
as well as cancerous.
Commenting on the breakthrough, University of Warwick researcher
and study co-author Dr Isolda Romero-Canelon said “The
energy-producing machinery in cancer cells works to the limit as
it attempts to keep up with quick proliferation and invasion. This
makes cancer cells susceptible to minor changes in the cell
‘power-house’. Our drug pushes cancer cells over the limit causing
them to slow and shut down, whilst normal cells can cope with its
effects”.
Preliminary data indicate that the novel drug may be ten times
more effective in treating ovarian, colon, melanoma, renal, and
some breast cancers, according to data obtained by the US National
Cancer Institute. The researchers now aim to expand the study to
cancers that are inherently resistant to existing drugs and to
those which have developed resistance after a first round of
chemotherapy treatments.
Study co-author Professor Peter J. Sadler said “Existing cancer
treatments often become less effective after the first course, as
cancer cells learn how they are being attacked. The drug we have
developed is a catalyst and is active at low doses. It can attack
cancer cells in multiple ways at the same time, so the cancer is
less able to adapt to the treatment. This means the new drugs
could be much more effective than existing treatments.”
“Platinum-based drugs are used in nearly 50% of all
chemotherapeutic regimens, exert their activity by damaging DNA
and cannot select between cancerous and non-cancerous cells,
leading to a wide-range of side-effects from renal failure to
neurotoxicity, ototoxicity, nausea and vomiting.
“In contrast, the new iridium-based drug is specifically designed
not to attack DNA, but to have a novel mechanism of action,
meaning that it could not only dramatically slow down and halt
cancer growth, but also significantly reduce the side effects
suffered by patients” argues Professor Sadler.
This research could also lead to substantial improvements in
cancer survival rates. “Current statistics indicate that one in
every three people will develop some kind of cancer during their
life time, moreover approximately one woman dies of ovarian cancer
every two hours in the UK according to Cancer Research UK .It is
clear that a new generation of drugs is necessary to save more
lives and our research points to a highly effective way of
defeating cancerous cells” said Dr Romero-Canelon.
http://onlinelibrary.wiley.com/doi/10.1002/anie.201311161/abstract;jsessionid=487D95E3B88B65F3288F6BC1F5D4638E.f01t03
Angewandte Chemie International Edition, Vol. 53 Issue 13
DOI: 10.1002/anie.201311161
11 MAR 2014
The Potent Oxidant Anticancer Activity
of Organoiridium Catalysts
Dr. Zhe Liu, Dr. Isolda Romero-Canelón, Bushra Qamar, Jessica
M. Hearn, Dr. Abraha Habtemariam, Dr. Nicolas P. E. Barry, Dr.
Ana M. Pizarro, Dr. Guy J. Clarkson and Prof. Dr. Peter J.
Sadler
Abstract
Platinum complexes are the most widely used anticancer drugs;
however, new generations of agents are needed. The
organoiridium(III) complex [(?5-Cpxbiph)Ir(phpy)(Cl)] (1-Cl),
which contains p-bonded biphenyltetramethylcyclopentadienyl
(Cpxbiph) and C^N-chelated phenylpyridine (phpy) ligands,
undergoes rapid hydrolysis of the chlorido ligand. In contrast,
the pyridine complex [(?5-Cpxbiph)Ir(phpy)(py)]+ (1-py) aquates
slowly, and is more potent (in nanomolar amounts) than both 1-Cl
and cisplatin towards a wide range of cancer cells. The pyridine
ligand protects 1-py from rapid reaction with intracellular
glutathione. The high potency of 1-py correlates with its ability
to increase substantially the level of reactive oxygen species
(ROS) in cancer cells. The unprecedented ability of these iridium
complexes to generate H2O2 by catalytic hydride transfer from the
coenzyme NADH to oxygen is demonstrated. Such organoiridium
complexes are promising as a new generation of anticancer drugs
for effective oxidant therapy.
NOVEL IRIDIUM/RHODIUM ANTI-CANCER COMPOUNDS
US2013065864
[ Excerpt ]
Inventor: HABTEMARIAM ABRAHA/LIU ZHE [GB] (+3)
Also published as: WO2011148124 / EP2575801 /
CN102905705 / CA2797921 / AU2011257002
BACKGROUND OF THE INVENTION
[0002] A significant development of organometallic chemistry in
recent years has been the increasing use of
pentamethylcyclopentadienyl compounds. Not only are such compounds
usually more soluble in organic solvents and more readily
crystallized than their unsubstituted cyclopentadienyl analogs,
but they are generally more stable as a result of the steric and
electron-donation effects of the five methyl groups. This is
particularly so for the
([eta]<5>-pentamethylcyclopentadienyl)iridium complexes,
where the [eta]<5>-C5Me5 acts as an excellent ligand toward
Ir(III) since it is displaced only with considerable
difficulty.<1 >
[0003] Sheldrick's group in Germany has studied the biological
activity of ([eta]<5>-pentamethyl cyclopentadienyl)iridium
complexes with polypyridyl ligands. Their work focuses on the
intercalative binding properties of polypyridyl (pp) ligands
(pp=dpq, dppz and dppn) into DNA. Recently they have showed that
[([eta]<5>-C5Me5)IrCl(dppz)](CF3SO3) and
[([eta]<5>-C5Me5)Ir((NMe2)2CS)(dppn)](CF3SO3)2 possess in
vitro cytotoxic activity towards MCF-7 and HT-29 cancer cell
lines, while [([eta]<5>-C5Me5)Ir(phen)Cl](CF3SO3) and
[([eta]<5>-C5Me5) Ir(en)Cl](CF3SO3) are inactive against
MCF-7 (breast cancer).<2 >Furthermore they have studied the
influence of polypyridyl ligands (pp=dpq, dppz and dppn) and
monodentate ligands (L-Cl, (NH2)2CS, (NMe2)2CS) on DNA
intercalation (see FIG. 1).<3 >They also found that the
complexes [IrCl3(DMSO)(pp)] (pp=phen, dpq, dppz, dppn), (FIG. 1),
are potent cytotoxic agents toward the human cell lines MCF-7 and
HT-29 and their IC50 values are dependent on the size of the
polypyridyl ligands.<4 >Their work on iridium and rhodium
polypyridyl complexes of general formula [Me(hal)3(sol)(pp)], in
which hal is a halogenide and sol is a solvent, is described in
EP2072521.
[0004] DNA binding of the type
[([eta]<5>-C5Me5)Ir(Aa)(dppz)](CF3SO3)n containing
S-coordinated amino acids has been studied and X-ray structure of
[([eta]<5>-C5Me5)Ir(9-EtG)(phen)](CF3SO3)2 has been
reported.<5 >
[0005] The biological activity of three novel indium(III)
complexes with 1,2-naphthoquinone-1-oximato ligand are also
described.<6 >The complex [([eta]<5>-C5Me5)Ir
(pyTz)Cl]<+ >containing the 2-(pyridine-2-yl)thiazole (pyTz)
N,N-chelating ligand is reported to be inactive towards human
ovarian cancer cell lines A2780 and A2780cisR
(cisplatin-resistant).<7 >
SUMMARY OF THE INVENTION
[0006] The present invention is based on studies on for
monofunctional Ir<III >complexes
[([eta]<5>-Cp<X>)Ir(LL)Cl]<0/+>, in which
Cp<X>=Cp*,
[eta]<5>-tetramethyl(phenyl)cyclopentadienyl (Cp<xph>)
and /7<6>-tetramethyl(biphenyl)cyclopentadienyl
(Cp<xbiph>) ligands (Chart 1), and the LL is an N,N-bound
ethylenediamine, 2,2'-bipyridine, 1,10-phenanthroline, N,O-bound
picolinate ligand, O,O-bound acetylacetonate (acac) ligand and
C,N-bound ligands. The rate of hydrolysis, acidity of the aqua
adducts, interactions with nucleobases, the uptake and
partitioning of these complexes in cells and relationship to
cancer cell cytotoxicity have been studied.
[0007] Without wishing to be bound by theory, it has been observed
that certain substituents on the cyclopentadienyl ring
significantly enhance cancer cell cytotoxicity, in particular the
phenyl substituents in [eta]<5>-tetramethyl(phenypcyclopenta
dienyl (Cp<xph>) and
[eta]<5>-tetramethyl(biphenyl)cyclopentadienyl
(Cp<xbiph>) ligands...
[0072] Examples of cancers which may be treated by the active
compounds include, but are not limited to, a carcinoma, for
example a carcinoma of the bladder, breast, colon (e.g. colorectal
carcinomas such as colon adenocarcinoma and colon adenoma),
kidney, epidermal, liver, lung, for example adenocarcinoma, small
cell lung cancer and non-small cell lung carcinomas, oesophagus,
gall bladder, ovary, pancreas e.g. exocrine pancreatic carcinoma,
stomach, cervix, thyroid, prostate, or skin, for example squamous
cell carcinoma; a hematopoietic tumour of lymphoid lineage, for
example leukemia, acute lymphocytic leukemia, B-cell lymphoma,
T-cell lymphoma, Hodgkin's lymphoma, non-Hodgkin's lymphoma, hairy
cell lymphoma, or Burkett's lymphoma; a hematopoietic tumor of
myeloid lineage, for example acute and chronic myelogenous
leukemias, myelodysplastic syndrome, or promyelocytic leukemia;
thyroid follicular cancer; a tumour of mesenchymal origin, for
example fibrosarcoma or habdomyosarcoma; a tumor of the central or
peripheral nervous system, for example astrocytoma, neuroblastoma,
glioma or schwannoma; melanoma; seminoma; teratocarcinoma;
osteosarcoma; xenoderoma pigmentoum; keratoctanthoma; thyroid
follicular cancer; or Kaposi's sarcoma.
[0073] Preferred cancers include leukaemia, CNS cancer, melanoma,
prostrate cancer, colon cancer, breast cancer or any selection
thereof.
Osmium (ii) arene azo anti-cancer complexes
CN103108880
Inventor: FU YING / SADLER PETER JOHN (+1)
Vacquinol-1 vs Cancer
http://www.sciencedaily.com/releases/2014/03/140320121906.htm
March 20, 2014
New approach makes cancer cells
explode
Researchers have discovered that a substance called Vacquinol-1
makes cells from glioblastoma, the most aggressive type of brain
tumor, literally explode. The established treatments that are
available for glioblastoma include surgery, radiation and
chemotherapy. But even if this treatment is given the average
survival is just 15 months. It is therefore critical to find
better treatments for malignant brain tumors.
Researchers at Karolinska Institutet in Sweden have discovered
that a substance called Vacquinol-1 makes cells from glioblastoma,
the most aggressive type of brain tumour, literally explode. When
mice were given the substance, which can be given in tablet form,
tumour growth was reversed and survival was prolonged. The
findings are published in the journal Cell.
The established treatments that are available for glioblastoma
include surgery, radiation and chemotherapy. But even if this
treatment is given the average survival is just 15 months. It is
therefore critical to find better treatments for malignant brain
tumours.
Researchers at Karolinska Institutet and colleagues at Uppsala
University have discovered an entirely new mechanism to kill
tumour cells in glioblastoma. Researchers in an initial stage have
exposed tumour cells to a wide range of molecules. If the cancer
cells died, the molecule was considered of interest for further
studies, which initially applied to over 200 kinds of molecules.
Following extensive studies, a single molecule has been identified
as being of particular interest. The researchers wanted to find
out why it caused cancer cell death.
It was found that the molecule gave the cancer cells an
uncontrolled vacuolization, a process in which the cell carries
substances from outside the cell into its interior. This carrying
process is made via the vacuoles, which can roughly be described
as blisters or bags consisting of cell membranes. The process is
similar to what was behind last year's Nobel Prize in physiology
or medicine, the discovery that describes how cellular vesicles
move things from the interior of the cell to its surface.
When cancer cells were filled with a large amount of vacuoles, the
cell membranes (the outer wall of the cell) collapsed and the cell
simply exploded and necrotized.
"This is an entirely new mechanism for cancer treatment. A
possible medicine based on this principle would therefore attack
the glioblastoma in an entirely new way. This principle may also
work for other cancer diseases, we have not really explored this
yet," says Patrik Ernfors, professor of tissue biology at the
Department of Medical Biochemistry and Biophysics at Karolinska
Institutet.
Researchers made mice that had human glioblastoma cells
transplanted ingest the substance for five days. The average
survival was about 30 days for the control group that did not
receive the substance. Of those who received the substance six of
eight mice were still alive after 80 days. The study was then
considered of such interest that the scientific journal wanted to
publish the article immediately.
"We now want to try to take this discovery in basic research
through preclinical development and all the way to the clinic. The
goal is to get into a phase 1 trial," says Patrik Ernfors.
The study has been funded with money from the Swedish Research
Council, the Swedish Cancer Society, the Swedish Foundation for
Strategic Research, the Brain Foundation, Hållsten's Research
Foundation, the Torsten Söderberg Foundation, and Wallenberg
Scholar.
Journal Reference:
Cell, 20 March 2014
DOI:
10.1016/j.cell.2014.02.021
Vulnerability of Glioblastoma Cells to
Catastrophic Vacuolization and Death Induced by a Small
Molecule.
Satish Srinivas Kitambi, et al.
Cancer Apoptosis by CD95
http://www.sciencedaily.com/releases/2014/03/140321095508.htm
March 21, 2014
Surprising new way to kill cancer
cells
Cancer cells -- and not normal cells -- can be killed by
eliminating either the FAS receptor, also known as CD95, or its
binding component, CD95 ligand, scientists have demonstrated. The
discovery seems counterintuitive because CD95 has previously been
defined as a tumor suppressor. To confirm the importance of CD95
for the survival of cancer cells in vivo, the researchers removed
it from tissues in animal models and found that cancer could not
form.
Northwestern Medicine scientists have demonstrated that cancer
cells -- and not normal cells -- can be killed by eliminating
either the FAS receptor, also known as CD95, or its binding
component, CD95 ligand.
"The discovery seems counterintuitive because CD95 has previously
been defined as a tumor suppressor," said lead investigator Marcus
Peter, professor in medicine-hematology/Oncology at Northwestern
University Feinberg School of Medicine. "But when we removed it
from cancer cells, rather than proliferate, they died."
The findings were published March 20 in Cell Reports.
The self-destruction of cells, known as apoptosis, is a necessary
process that helps the body rid itself of unwanted and potentially
harmful cells. Under normal circumstances, when CD95 is activated,
the process of apoptosis is triggered. Seen as a keeper of
homeostasis in the immune system, it's been long-considered vital
for the prevention of uncontrolled, cancerous cell growth.
"In order to conduct this line of work, we had to create something
that I don't believe exists, a cancer cell completely devoid of
CD95," said Peter, a member of the Robert H. Lurie Comprehensive
Cancer Center of Northwestern University. "If CD95 was truly a
tumor suppressor, its elimination would result in an enhanced
growth and/or invasiveness of cancer cells."
Peter and his team tested cancer cells from nine different tissue
origins. Instead of proliferating, the cells increased their size
and the production of harmful reactive oxygen species, resulting
in DNA damage. In their first attempt to divide, they died.
Peter determined that the "cell death induced by CD95 receptor or
ligand elimination (DICE)," comprises multiple death pathways. A
cancer cell would have to mutate components of each to defend
against DICE, a highly unlikely scenario.
"DICE killed every cancer cell we put it up against and we found
nothing that could prevent its destruction," Peter said. "The fact
that none of the more than 1,000 drugs, nor the knockdown of any
single gene was found to counteract DICE, makes it a very
promising new way to kill cancer cells."
To confirm the importance of CD95 for the survival of cancer cells
in vivo, Peter and colleagues removed it from tissues in animal
models and found that cancer could not form.
"We know CD95 is not essential for the survival of any tissue
outside of the immune system because mice with a deletion of
either CD95 or CD95 ligand complete an average lifecycle with no
illness other than autoimmunity," he said.
The findings suggest that dependence on CD95 and CD95 ligand for
survival is a feature of cancer cells that distinguishes them from
normal cells.
"We didn't believe these findings at first, but after more than
four years of detailed experiments, we have convinced ourselves
and others that what we have shown reflects reality," Peter said.
Peter is now working with Chad Mirkin, the George B. Rathmann
Professor of Chemistry in the Weinberg College of Arts and
Sciences and professor of medicine at Feinberg, to induce DICE in
cancer cells using small interfering RNAs delivered by gold
nanoparticles.
"We're not going to reinvent the wheel," Peter said. "Alexander
Stegh, assistant professor of neurology and of medicine at
Feinberg, has already used the same nano-platform to target a gene
in a mouse model for brain cancer. In developing nano-DICE, we can
begin the process of finding new treatment options."
Journal Reference:
Cell Reports, March 2014
DOI:
10.1016/j.celrep.2014.02.035
Death Induced by CD95 or CD95 Ligand
Elimination.
Abbas Hadji, et al.
Magnesium Chloride Potentiation of
Solar Cells
http://www.independent.co.uk/news/science/breakthrough-in-solar-panel-manufacture-promises-cheap-energy-within-a-decade-9563136.html
25 June 2014
Breakthrough in solar panel
manufacture promises cheap energy within a decade
Technical advance based on edible salt overcomes need to use
toxic agents
by
Steve Connor
A breakthrough in the production of solar cells will make the next
generation of solar panels cheaper and safer, and promises to
accelerate the development of solar energy over the next decade,
scientists said.
A technical advance based on an edible salt used in the
manufacture of tofu could revolutionise the production of future
solar panels to make them less expensive, more flexible and easier
to use than the current models seen on millions of roofs across
Britain.
Researchers believe they have found a way of overcoming one of the
most serious limitations of the next generation of solar panels,
which are based on toxic cadmium chloride, by simply adding
magnesium chloride, an abundant salt found in seawater.
A study has shown that the solar cells produced with magnesium
chloride – which is also found in bath salts as well as used to
coagulate soya milk into tofu – work just as efficiently as
conventional cadmium cells but at a fraction of the cost and with
much lower toxicity.
“We certainly believe it’s going to make a big change to the costs
of these devices. The cost of solar is going to match fossil fuels
eventually but this is going to get us there quicker,” said Jon
Major of the University of Liverpool, who led the research.
“Magnesium chloride is incredibly low-cost and it’s simply
recovered from seawater. It’s used to de-ice roads in winter and
it’s completely harmless and non-toxic. We’ve managed to replace a
highly expensive, toxic material with one that’s completely benign
and low cost,” Dr Major said.
About 90 per cent of the solar panels currently in use are made of
photovoltaic cells composed of silicon semiconductors, which
convert sunlight directly into electricity. However, silicon is
not good at absorbing sunlight which is why the next generation of
PV cells will be based on a thin coating of cadmium telluride,
which absorbs sunlight so well that it only needs to be about one
hundredth of the thickness of silicon.
However, although cadmium telluride is seen as the future for
solar energy, it is potentially dangerous after it is “activated”
with cadmium chloride, a critical step in the manufacturing
process that raises the efficiency of converting sunlight to
electricity from about two per cent to 15 per cent or more.
The Liverpool team attempted to find an alternative to cadmium
chloride in the activation step and discovered that it could be
done just as well with magnesium chloride, which they sprayed onto
a test sample of cadmium telluride with a model aircraft spray gun
they bought for £49.99, Dr Major said.
In a study published in the journal Nature, the researchers
demonstrated that the efficiency of the resulting photovoltaic
cells made from cadmium telluride and magnesium chloride were on a
par with commercial cadmium telluride cells that had been
activated with toxic cadmium chloride.
“We have to apply cadmium chloride in a fume cupboard in the lab,
but we created solar cells using the new method on a bench with a
spray gun bought from a model shop,” Dr Major said.
“Cadmium chloride is toxic and expensive, and we no longer need to
use it. Replacing it with a naturally occurring substance could
save the industry a vast amount of money and reduce the overall
cost for generating power from solar,” he said.
It is not possible to estimate how much cheaper the new solar
cells will be, Dr Major said, but magnesium chloride is about one
per cent of the cost of cadmium chloride. In addition, waste
disposal will be far easier and cheaper with a product based on a
non-toxic salt, he said.
Asked why the solar power industry had not thought of using
magnesium chloride before, Dr Major said: “We genuinely don’t
know. The only reason we can suggest is that cadmium chloride
works well so it may be a case of ‘if it’s not broke, why is there
a need to fix it?’”
Jeremy Leggett, chairman of the renewable energy firm
Solarcentury, said that the development is exciting because it
promises to make an already competitive industry even more
competitive with conventional sources of energy, such as fossil
fuels.
“Their costs are coming down so fast that they are already
knocking the business models of utilities into what some analysts
call a ‘death spiral’. Imagine, then, what will happen if
developments such as the one described in the new research come to
market,” Dr Leggett said.
Just for Flatulation & Giggles Department :
Martin POHLMAN : Time Machine
US2006073976
Method of gravity distortion and time displacement
Abstract
A method for employing sinusoidal oscillations of electrical
bombardment on the surface of one Kerr type singularity in close
proximity to a second Kerr type singularity in such a method to
take advantage of the Lense-Thirring effect, to simulate the
effect of two point masses on nearly radial orbits in a 2+1
dimensional anti-de Sitter space resulting in creation of circular
timelike geodesics conforming to the van Stockum under the Van Den
Broeck modification of the Alcubierre geometry (Van Den Broeck
1999) permitting topology change from one spacelike boundary to
the other in accordance with Geroch's theorem (Geroch 1967) which
results in a method for the formation of Godel-type geodesically
complete spacetime envelopes complete with closed timelike curves.
FIELD OF THE INVENTION
[0001] The present invention relates to the use of technical time
displacement devices, which operate by the modification of
gravitational fields. These drive systems do not depend on the
emission of matter to create thrust to take advantage of time
dilation, but rather create a change in the curvature of
space-time, in accordance with general relativity. This allows
travel across topologies by warping space-time, to produce a
topology change from one spacelike boundary to the other in
accordance with Geroch's theorem (Geroch 1967)
THEORETICAL BACKGROUND OF THE INVENTION
[0002] The concept of gravity should be examined in the light of
quantum gravity and in turn as a component of quantum physics
itself. The fundamental minimal quantum of energy in quantum
physics is Planck's constant; h. Thus in accordance with the
energy equivalence formula E=mc<2> , the fundamental minimum
quantity of mass (mq) can therefore be derived, from known
constants by; mq=h/c<2 > (1). Taking this minimal mass, it
is possible to show that the formation of all matter, the forces
of nature and indeed space-time itself derive from this single
quintessential quantity.
[0003] Thus if the number of quintessences in a system is;
nq=m/mq: then the total Energy of the system is more logically
given by, the energy of a single quintessence (h); directly
multiplied by the number of quintessences (nq) in that system,
thus
E=hnq=mc<2> (1 a).
[0004] Furthermore, this minimal mass, termed quintessence, can
form the basis of the existence of a quantum gravitational field
in the form of a space-time lattice, from which quantum gravity
may be derived from first principles. Furthermore, the
conglomeration of these quintessences also accounts for the
formation of the elementary particles and the forces acting
between them, as in superstring theory. This concept explains the
formation of matter and the forces of nature on a quantum
mechanical basis and directly explains the existence of wave
particle duality. Thus as nq=m/mq; the frequency of light and
matter (f) is determined, directly, from the number of constituent
quintessences. This leads automatically to the fundamental
equation, derived from (1), f=nq=E/h, where nq is the number of
quintessences, which leads directly to the frequency of both light
and matter. This in turn leads directly to a Universal wave
equation for matter and light [lambda]=c/[beta]nq=hc/[beta]E (2),
where [beta] is the relative directional velocity, v/c. As the
momentum, p=[beta]*E/c, then this equation also gives the standard
de-Broglie wave equation, [lambda]=h/p in agreement with current
theory and experiments<1> .
[0005] Using the Universal wave equation, the standard equation
for special relativity, m'=mo/(1-[beta]<2> )<1/2> ,
derives from first principles. Also from these observations, a
modified Dirac wave equation may be derived,
E[psi]=(-j[beta].[Nabla]+[beta]m)[psi] (2a), the results of which
have been recently verified by a paper in which the orbitals of
electrons were experimentally directly visualised<2> .
Moreover, a fundamental equation for general relativity can be
formulated, where G is the gravitational constant and rq is the
given radius of quintessence; G=9(rq)<2> c<4>
/[lambda][beta]E (3), such that the Universal wave equation is in
direct agreement with general relativity<3> . Thus special
and general relativity and quantum mechanics can be unified.
[0006] From here it is possible to proceed in a number of ways;
the geometric structure of the electron and the forces of Nature
may be derived from first principles and in turn the structure of
the quarks, including the top and bottom, otherwise known as truth
and beauty can be seen. Moreover, the presence of a space-time
lattice results in an understanding of quantum EPR effects. By
allowing a theoretical flow of energy through the space-time
lattice it can be shown that:
[0007] Energy is not bound by space-time
[0008] Thus logically accounting for phenomena such as
entanglement and quantum tunnelling. Quintessence can also be used
to explain, logically, the inner physics of a black hole, the
missing mass of the Galaxy, the continuing expansion of the
Universe, Guth's inflationary theory and the Big Bang. Hence, it
is now possible to understand the Universe, including space-time,
matter and the forces of nature from the radius, mass and
vibration of a single quantity, quintessence.
[0009] With this understanding of space-time, matter and the
forces of Nature, and in particular gravity, it is possible to
demonstrate that the modification of gravitational fields, and in
turn the warping of space-time, can be technically readily
achieved.
[0010] Using standard equations for special relativity,
m'=m0/(1-[beta]<2> )<1/2> , it can be demonstrated
that by differentially increasing the velocity of electrons, by
applying a differential current, their mass can be increased in a
specific way. In turn by increasing the mass of electrons, by
general relativity, the number of gravitons emitted from these
electrons can be modulated. By multiplying this effect using an
ultracentrifugational device the differential graviton emission
can be manifestly amplified. This in turn, in accordance with
general relativity, will cause a change in the curvature of
space-time.
[0011] This effective warping of space-time does not, of
necessity, imply superluminal velocities, but does allow the
creation of warp drive systems, which do not depend on the
creation of thrust by the ejection of material as used in current
space technologies.
Part 1 - Fundamental Laws of Physics
[0012] Quintessential Mass
[0013] The quantum physical, minimum component of energy is
Planck's constant; h. To define the minimal component of mass,
using the standard energy equivalence formula; E=mc<2> ,
such a minimal mass (mq) would be required to have the value
equivalent to; mq=h/c<2 > (1). The total mass of a system
(m) would then be; m=nqmq, where (nq) is the number of these
minimal units. Thence, the total energy of a system can be derived
from the minimal energy; h, multiplied by the number of these
energy units (nq). Thus as, E=mc<2> , then also E=mqnqc<2
> and substituting mq=h/c<2> , the energy equivalence
formula has the more logical formulation; E=hnq(1a). Thus the
energy of a system is equivalent to the minimal energy unit; h,
multiplied by the number of those minimal energy units (nq).
[0014] Taking this minimal mass/energy, it is possible to show
that all matter, the forces of nature and space time can be
constructed from this single quintessential quantity. Moreover,
using this quantity the laws of physics can be derived from first
principles. Thus, a priori, all components of the physical
universe, including space-time, can be constructed from this
minimal mass component, termed quintessence...
&c...
[0015] Wave Particle Duality
[0027] Wave Equations
[0050] Wave Particle Duality and Relativity
[0057] The Space-Time Lattice
[0072] Quintessence and Complex Space
[0078] The Three Dimensional Argand Diagram
[0081] Energy and the Space-Time Lattice
[0086] Energy is Not Bound by the Space-Time Lattice
Part II-Particle Physics
[0092] Electron Structure
[0105] Complex Space and Electron Structure
[0115] Electron Pairing and Superconductivity
[0121] The Fine Structure Constant
[0125] Fundamental Forces and Particle Structure
[0165] Particle Spin and Size
Part III - Quantum Gravity
[0187] Quantum General Relativity
[0212] Quantum Gravity and Wave Particle Duality
[0231] Graviton Structure
[0236] Quantised General Relativity
[0248] Graviton Force Characteristics
[0252] Quantum Gravity and Electromagnetism
[0267] Quantum Gravity and the Charge of the Electron
[0285] Quantum Gravity and the Electron Magnetic Moment
[0300] Quantum Gravity and Special Relativity
[0309] Quintessence and Black Holes
[0323] Quintessence and the Big Bang
[0337] The Nature of Energy
[0345] Energy is not Bound by the Space-Time Lattice
[0350] Part IV: Applied Theory with the Intent to Create Closed
Timelike Curves
[0351] Electron Bombardment of the Photosphere to Induce
Gravitational Shift
[0355] Stable CTC Solution From Modified M-Theory
SUMMARY OF THE INVENTION
[0360] The present invention is A method for the generation of a
pseudo 2+1 dimensional anti-de Sitter space (DeDeo & Gott
2002) using two Kerr type positively charged rotating dilation
singularities where one singularity is maintained as a axis of
rotation or "reference" singularity, and the other "target"
singularity is subjected to a differential electron flow so as to
simultaneously pass above the photosphere of said singularity in
its direction of rotation-prograde orbit-and contrary to its
direction of rotation-retrograde orbit-to release a directed flow
of gravitons in a sinusoidal oscillation simulating a rotational
effect of the "target" singularity around the axis of rotation
provided by the "reference" singularity, resulting in the creation
of timelike curves in a compact time-oriented manifold permitting
topology change from one spacelike boundary to the other in
accordance with Geroch's theorem (Geroch 1967) which results in a
method for the formation of G odel-type geodesically complete
spacetime envelopes complete with closed timelike curves.
BRIEF DESCRIPTION OF THE DRAWINGS
[0361] FIG. 1 is a schematic representation of the mechanism
employed to house the components necessary to generate a 2+1
dimensional anti-de Sitter space, resulting in the creation of
timelike curves in a compact time-oriented manifold
[0362] FIG. 2 is a schematic representation of the G
odel-type geodesically complete spacetime envelope created by
the mechanism complete with closed timelike curves
John LILLY : Balanced Pulse-Pair
Waveform
[ The "Lilly Wave ' ]
[ PDF ]
10 Search Engines for Exploring of the
Deep / Invisible Web
Infomine
http://infomine.ucr.edu/
The WWW Virtual Library
http://vlib.org/
Intute
http://www.intute.ac.uk/
Complete Planet
www.http://aip.completeplanet.com/
Infoplease
http://www.infoplease.com/index.html
DeepPeep
www.deeppeep.org
IncyWincy
http://www.incywincy.com/
DeepWebTech
http://www.deepwebtech.com/
Scirus
www.scirus.com
TechXtra
ww.techxtra.ac.uk/index.html
Fasting vs Cancer
https://news.usc.edu/63669/fasting-triggers-stem-cell-regeneration-of-damaged-old-immune-system/
Fasting triggers stem cell regeneration of
damaged, old immune system
Protection from chemotherapy immunosuppression indicates effect
could be conserved in humans
In the first evidence of a natural intervention triggering stem
cell-based regeneration of an organ or system, a study in the June
5 issue of the Cell Stem Cell shows that cycles of prolonged
fasting not only protect against immune system damage — a major
side effect of chemotherapy — but also induce immune system
regeneration, shifting stem cells from a dormant state to a state
of self-renewal.
In both mice and a Phase 1 human clinical trial involving patients
receiving chemotherapy, long periods of not eating significantly
lowered white blood cell counts. In mice, fasting cycles then
“flipped a regenerative switch,” changing the signaling pathways
for hematopoietic stem cells, which are responsible for the
generation of blood and immune systems, the research showed.
The study has major implications for healthier aging, in which
immune system decline contributes to increased susceptibility to
disease as people age. By outlining how prolonged fasting cycles —
periods of no food for two to four days at a time over the course
of six months — kill older and damaged immune cells and generate
new ones, the research also has implications for chemotherapy
tolerance and for those with a wide range of immune system
deficiencies, including autoimmunity disorders.
“We could not predict that prolonged fasting would have such a
remarkable effect in promoting stem cell-based regeneration of the
hematopoietic system,” said corresponding author Valter Longo,
Edna M. Jones Professor of Gerontology and the Biological Sciences
at the USC Davis School of Gerontology and director of the USC
Longevity Institute. Longo has a joint appointment at the USC
Dornsife College of Letters, Arts and Sciences.
“When you starve, the system tries to save energy, and one of the
things it can do to save energy is to recycle a lot of the immune
cells that are not needed, especially those that may be damaged,”
Longo said. “What we started noticing in both our human work and
animal work is that the white blood cell count goes down with
prolonged fasting. Then when you re-feed, the blood cells come
back. So we started thinking, well, where does it come from?”
Fasting cycles
Prolonged fasting forces the body to use stores of glucose, fat
and ketones, but it also breaks down a significant portion of
white blood cells. Longo likens the effect to lightening a plane
of excess cargo.
During each cycle of fasting, this depletion of white blood cells
induces changes that trigger stem cell-based regeneration of new
immune system cells. In particular, prolonged fasting reduced the
enzyme PKA, an effect previously discovered by the Longo team to
extend longevity in simple organisms and which has been linked in
other research to the regulation of stem cell self-renewal and
pluripotency — that is, the potential for one cell to develop into
many different cell types. Prolonged fasting also lowered levels
of IGF-1, a growth-factor hormone that Longo and others have
linked to aging, tumor progression and cancer risk.
“PKA is the key gene that needs to shut down in order for these
stem cells to switch into regenerative mode. It gives the OK for
stem cells to go ahead and begin proliferating and rebuild the
entire system,” explained Longo, noting the potential of clinical
applications that mimic the effects of prolonged fasting to
rejuvenate the immune system. “And the good news is that the body
got rid of the parts of the system that might be damaged or old,
the inefficient parts, during the fasting. Now, if you start with
a system heavily damaged by chemotherapy or aging, fasting cycles
can generate, literally, a new immune system.”
Prolonged fasting also protected against toxicity in a pilot
clinical trial in which a small group of patients fasted for a
72-hour period prior to chemotherapy, extending Longo’s
influential past research.
“While chemotherapy saves lives, it causes significant collateral
damage to the immune system. The results of this study suggest
that fasting may mitigate some of the harmful effects of
chemotherapy,” said co-author Tanya Dorff, assistant professor of
clinical medicine at the USC Norris Comprehensive Cancer Center
and Hospital. “More clinical studies are needed, and any such
dietary intervention should be undertaken only under the guidance
of a physician.”
“We are investigating the possibility that these effects are
applicable to many different systems and organs, not just the
immune system,” said Longo, whose lab is in the process of
conducting further research on controlled dietary interventions
and stem cell regeneration in both animal and clinical studies.
The study was supported by the National Institute of Aging of the
National Institutes of Health (grant numbers AG20642, AG025135,
P01AG34906). The clinical trial was supported by the V Foundation
and the National Cancer Institute of the National Institutes of
Health (P30CA014089).
Chia Wei-Cheng of USC Davis was first author of the study. Gregor
Adams, Xiaoying Zhou and Ben Lam of the Eli and Edythe Broad
Center for Regenerative Medicine and Stem Cell Research at USC;
Laura Perin and Stefano Da Sacco of the Saban Research Institute
at Children’s Hospital Los Angeles; Min Wei of USC Davis; Mario
Mirisola of the University of Palermo; Dorff and David Quinn of
the Keck School of Medicine of USC; and John Kopchick of Ohio
University were co-authors of the study.
http://www.sciencedaily.com/releases/2012/02/120208152254.htm
February 8, 2012
Fasting weakens cancer in mice
Summary:
New study finds that short fasting cycles can work as well as
chemotherapy, and the two combined greatly improve survival.
Man may not live by bread alone, but cancer in animals appears
less resilient, according to a study that found chemotherapy drugs
work better when combined with cycles of short, severe fasting.
Even fasting on its own effectively treated a majority of cancers
tested in animals, including cancers from human cells.
The study in Science Translational Medicine, part of the Science
family of journals, found that five out of eight cancer types in
mice responded to fasting alone: Just as with chemotherapy,
fasting slowed the growth and spread of tumors.
And without exception, "the combination of fasting cycles plus
chemotherapy was either more or much more effective than chemo
alone," said senior author Valter Longo, professor of gerontology
and biological sciences at the University of Southern California.
For example, multiple cycles of fasting combined with chemotherapy
cured 20 percent of mice with a highly aggressive type of
children's cancer that had spread throughout the organism and 40
percent of mice with a more limited spread of the same cancer.
No mice survived in either case if treated only with chemotherapy.
Only a clinical trial lasting several years can demonstrate
whether humans would benefit from the same treatment, Longo
cautioned.
Results from the first phase of a clinical trial with breast,
urinary tract and ovarian cancer patients, conducted at the USC
Norris Comprehensive Cancer Center and led by oncologists Tanya
Dorff and David Quinn, in collaboration with Longo, have been
submitted for presentation at the annual meeting of the American
Society of Cancer Oncologists.
The first phase tests only the safety of a therapy, in this case
whether patients can tolerate short-term fasts of two days before
and one day after chemotherapy.
"We don't know whether in humans it's effective," Longo said of
fasting as a cancer therapy. "It should be off limits to patients,
but a patient should be able to go to their oncologist and say,
'What about fasting with chemotherapy or without if chemotherapy
was not recommended or considered?"
In a case report study with self-reported data published in the
journal Aging in 2010, 10 cancer patients who tried fasting cycles
perceived fewer side effects from chemotherapy.
Longo stressed that fasting may not be safe for everyone. The
clinical trial did not enroll patients who already had lost more
than 10 percent of their normal weight or who had other risk
factors, such as diabetes. Fasting also can cause a drop in blood
pressure and headaches, which could make driving and other
activities dangerous for some patients.
In mice, the study found that fasting cycles without chemotherapy
could slow the growth of breast cancer, melanoma, glioma and human
neuroblastoma. In several cases, the fasting cycles were as
effective as chemotherapy.
Fasting also extended survival in mice bearing a human ovarian
cancer. In the case of melanoma, the cancer cells became resistant
to fasting alone after a single round, but the single cycle of
fasting was as effective as chemotherapy in reducing the spread of
cancer to other organs.
For all cancers tested, fasting combined with chemotherapy
improved survival, slowed tumor growth and/or limited the spread
of tumors.
As with any potential cancer treatment, fasting has its limits.
The growth of large tumor masses was reduced by multiple fasting
and chemotherapy cycles, but cancer-free survival could not be
achieved. Longo speculated that cells inside a large tumor may be
protected in some way or that the variety of mutations in a large
mass may make it more adaptable.
But he noted that in most patients, oncologists have at least one
chance to attack the cancer before it grows too large.
Longo and collaborators at the National Institute on Aging studied
one type of breast cancer in detail to try to understand the
effects of fasting.
While normal cells deprived of nutrients enter a dormant state
similar to hibernation, the researchers saw that the cancer cells
tried to make new proteins and took other steps to keep growing
and dividing.
The result, Longo said, was a "cascade of events" that led to the
creation of damaging free radical molecules, which broke down the
cancer cells' own DNA and caused their destruction.
"The cell is, in fact, committing cellular suicide. What we're
seeing is that the cancer cell tries to compensate for the lack of
all these things missing in the blood after fasting. It may be
trying to replace them, but it can't," Longo said.
The new study bookends research published in Proceedings of the
National Academy of Sciences in 2008.
In that study, Longo's team showed that fasting protected normal
cells against chemotherapy, but did not address the effect on
cancer cells. The study also focused only on a single cancer and
chemotherapy drug.
The new study on a range of cancers and common chemotherapy drugs
extends the 2008 results by showing that fasting not only fails to
protect cancer cells, but makes them more vulnerable.
Longo called the effect "Differential Stress Sensitization" to
reflect the change in vulnerability between normal and cancerous
cells.
Longo's interest in fasting and cancer grew from years of studies
on the beneficial effects of fasting in yeast and other organisms.
He showed 15 years ago that starved yeast cells enter a
stress-resistant mode as they wait for better times.
By contrast, he said, the mutations in cancer cells come at a
cost, such as a loss in adaptability to diverse environments. For
example, Longo found that yeast genetically modified to resemble
cancer cells become much more sensitive to several toxins.
"A way to beat cancer cells may not be to try to find drugs that
kill them specifically but to confuse them by generating extreme
environments, such as fasting that only normal cells can quickly
respond to," Longo said...
Journal Reference:
Changhan Lee, Lizzia Raffaghello, Sebastian Brandhorst, Fernando
M. Safdie, Giovanna Bianchi, Alejandro Martin-Montalvo, Vito
Pistoia, Min Wei, Saewon Hwang, Annalisa Merlino, Laura Emionite,
Rafael de Cabo, and Valter D. Longo. Fasting Cycles Retard Growth
of Tumors and Sensitize a Range of Cancer Cell Types to
Chemotherapy. Science Translational Medicine, Feb 8, 2012 DOI:
10.1126/scitranslmed.3003293
http://www.nia.nih.gov/newsroom/announcements/2011/07/study-finds-fasting-may-help-reduce-negative-side-effects
July 28, 2011
Study finds fasting may help reduce
negative side effects of chemotherapy
Valter Longo and colleagues proposed that a treatment used to
prolong life in some laboratory organisms could offer protection
against the negative effects of chemotherapy. That treatment
is fasting, a special type of dietary restriction. Dietary
restriction provides adequate nutrition at lower-than-average
calories, either through special daily meals or intermittent
fasting.
In some of the earlier studies of dietary restriction in animal
models, researchers measured resistance to stress as a way of
predicting potential impact on lifespan and health.
Successful resistance to short-term stress caused by reduction in
calories typically correlates with longer life and better health.
Researchers have also found in some models that fasting for
relatively short periods of time – or months of dietary
restriction – actually enhanced normal cells’ resistance to
stress, but did not have an effect on cancer cells.
Based on these observations, Longo and colleagues hypothesized
that they could use this “differential stress resistance” induced
by fasting to reduce chemotherapy-related stress on normal cells,
without jeopardizing the treatment’s efficacy for killing
cancerous cells. Initial results in mice were encouraging: the
mice survived and the chemotherapy was still effective. A
subsequent but still very preliminary clinical study showed that
patients who fasted in conjunction with chemotherapy reported
fewer side-effects without loss of efficacy. The clinical study
has been expanded to an early phase clinical trial.
References:
Raffaghello L, et al. Fasting and differential chemotherapy
protection in patients. Cell Cycle 2010 9: 4474 – 4476.
Lee C, Longo VD. Fasting vs. dietary restriction in cellular
protection and cancer treatment: from model organisms to patients.
Oncogene 2011 30: 3305 – 3316.
http://www.cbc.ca/news/technology/scientists-say-nerves-use-sound-not-electricity-1.671526
Mar 09, 2007
Scientists say nerves use sound, not
electricity
The common view that nerves transmit impulses through electricity
is wrong and they really transmit sound,according to a team of
Danish scientists.
The Copenhagen University researchers argue that biology and
medical textbooks that say nerves relay electrical impulses from
the brain to the rest of the body are incorrect.
"For us as physicists, this cannot be the explanation," said
Thomas Heimburg, an associate professor at the university's Niels
Bohr Institute. "The physical laws of thermodynamics tell us that
electrical impulses must produce heat as they travel along the
nerve, but experiments find that no such heat is produced."
Heimburg, an expert in biophysics who received his PhD from the
Max Planck Institute in Goettingen, Germany — where biologists and
physicists often work together in a rare arrangement — developed
the theory with Copenhagen University's Andrew Jackson, an expert
in theoretical physics.
According to the traditional explanation of molecular biology, an
electrical pulse is sent from one end of the nerve to the other
with the help of electrically charged salts that pass through ion
channels and a membrane that sheathes the nerves. That membrane is
made of lipids and proteins.
Heimburg and Jackson theorize that sound propagation is a much
more likely explanation. Although sound waves usually weaken as
they spread out, a medium with the right physical properties could
create a special kind of sound pulse or "soliton" that can
propagate without spreading or losing strength.
The physicists say because the nerve membrane is made of a
material similar to olive oil that can change from liquid to solid
through temperature variations, they can freeze and propagate the
solitons.
The scientists, whose work is in the Biophysical Society's
Biophysical Journal,suggested that anesthetics change the melting
point of the membrane and make it impossible for their theorized
sound pulses to propagate.
The researchers could not immediately be reached for comment.