发信人: justacode (Hi), 信区: Biology
标 题: idea in questions
发信站: The unknown SPACE (Wed Jun 4 18:44:27 2003) WWW-POST

What confused me is localized cell death introduction (by many physical
methods or by pharmalogical methods, such as pathway blockage) is not always
generate amplified response of tumor rejection to the whole body.

Please contribute. The following containing direct up-lifting sentences.

3x

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Cell death introduction with immunotherapy
There are various ways to introduce localized cell death. The associate
immunology events are interested to look into. There might be ways to
introduce localized inflammations by molecular biology and by oxidation to
lipids radiated with electric magnetic field. Oxidation events are introduced
through immunology effecter cells and/or antibody. They are firstly controlled
by dendritic cells, to solid and none solid tumors. The tolerance events need
to overcome, so as to induce increased systemic tumor immunity, after
localized cell death induction. It is known that oxidation events around solid
tumors could be used. It seems that for none solid tumors, antibody could
introduce localized oxidation events to lipid membrane. Certain atomic index
could also be the target of electric magnetic field. Consequently, the
regulation of antibody production and immunity over tolerance are worth
looking into, so as to introduce tumor antigen to dendritic cells in vivo.
Introduction:
There are different types of cell deaths, with different antigen presenting
cell (APC) responses. Necrotic and apoptotic cell deaths triggered different
APC responses via different receptors, in vitro. It is pivotal to study them
in vivo or in situ, even though cell deaths, after classical radiation, are
mixed events of apoptosis and necrosis.

If cell damaging events can be triggered and maintained in a controllable and
localized manner, avoiding antigen-specific unresponsiveness or tolerance in
central lymphoid organs and periphery, immunotherapy will have a new spandrel,
especially for cancers without general specific antigens. “Heat shock protein
vaccines must be produced for each patient from that patients’ cancer.” This
is the practical difficulty in the clinical trials for none specific antigen
tumors, which can be solved by cell death introduction combining with
immunotherapy.

The localized inflammation and cell death can be introduced by electromagnetic
therapy, gene therapy and localized radiation. There might be ways to trigger
heat shock responses first and necrosis events second, in a controllable
manner, with in vivo target, either using atomic index of specific structure
(hydrogen associated with oxidation and nitration), or exploiting localized
radiation events. This notion is of physics basis, and biological
associations. It is easy to interpret the events by danger model.
Consequently, it is interesting to look into the regulation of antibody
production, and other in vivo epoxide targets generators’ function, so as to
either introduce electrofusion in vivo or upload DC with tumor cells in vivo;
it is also interesting to look into the in vivo effects of artificial
antibodies of the same internalization rate binding radiation material with
different penetration abilities. On the other hand, diverse stresses (heat,
ionizing radiation, ultraviolet light, chemotherapeutic agents, and oxidative
challenges) might generate expressions of materials in different condensed
states, and be accumulated and released following either reaction diffusion or
fractional diffusion model.

Transformation may be unleashed by defects in communication pathways
maintaining tissue homeostasis. The other consideration is a neglect of immune
surveillance system to this action. Traditional way to study protein-protein
interactions is blotting. Kinetic models are involved. Protein array is
developing in phosphorylation events, and protein-protein interactions without
additional labeling steps of probe proteins.

Life science research is vital not just to biotechnology companies and their
investors, but to all human beings as a whole. By structuring the common sense
that only those with private funds or a commercial motive do the pioneering
work, many researchers curb their full capacity to expand our scientific
understandings and collaborations.
There are ways to introduce localized damage
Our understanding of cell death in health and disease is far from complete,
and the challenge of converting that understanding into new treatment plans is
at the starting point. Therapeutic strategies designed to modulate cell death
hold significant clinical promise, as a number of diseases have been linked to
abnormalities in the occurrence of cell death. In vitro models where apoptosis
was inhibited by one means or another, the cells eventually succumbed to a
nonapoptotic type of death resembling necrosis.

With the development of technology, radiation events are relatively localized
to the targets. There are observations of immunology players’ recruitment,
which was not observed in non-irradiated tumors. Consequently, in situ study
of immunology events and player recruitments of solid tumor in long term study
would be interesting. MicroPET scanner enables observations of small animals
in signal animal, long terms and of three dimensional. For several years,
Curley developed preclinical studies and clinical studies, using
radiofrequency ablation (RFA) for thermal destruction of primary and
metastatic liver tumors. RFA is a technology that can be applied to
unresectable hepatic malignancies without significant morbidity and with
limitations of accurate localizations as most techniques of that field. There
are other physical methods to introduce localized damage, such as interstitial
laser-induced thermotherapy (LITT). In the epoxide group targeted studies,
using different principles, some solid tumors and none solid tumors could
generate good responses. That made the consideration that antibody
specifically introducing damage events to the none-solid tumors as an
interesting hypothesis.

Monoclone antibody (mAb) could be used to for targeting. One targeting device
is by use of a generic antibody molecule that forms a covalent bond with a
1,3-diketone functionality, essentially any compound can be turned into an
immunotherapeutic agent, thereby not only increasing the diversity space that
can be accessed but also multiplying the therapeutic effect. Another targeting
device is using mAb binding to particles instead of -emitting isotopes.
Because of their long range, particles can lead to the destruction of
targeted cells and surrounding tumor cells, which can also result in the
killing of normal bystander cells, such as immunology factors. In contrast,
particles are high-energy helium nuclei with short path lengths. The linear
energy transfer of particles is much greater than that of particles.
Injured cells have limited chances to repair DNA damage induced by
particles, and cell death may result from a single atomic decay traversing the
nucleus. Therefore, radioimmunotherapy with particle-emitting isotopes (Ac)
may produce more efficient killing of individual tumor cells with little
damage to surrounding normal tissues than long path lengths particles. The
considerations of using in vivo antibody’s catalytic activity in response to
out field for none solid tumor treatment is something new and waiting for
tests in none solid tumor models. Solid tumors are invariably less well
oxygenated than normal tissues. Prolonged hypoxia of the tumor tissue also
leads to necrosis, and necrotic regions are also characteristic of solid
tumors. These two characteristics (hypoxia and necrosis) represent clear
differences between tumors and normal tissues. They are potentially
exploitable in cancer treatment.

Attention has focused on the ability of dendritic cells (DC) as professional
APC capable of eliciting T and B cell mediated responses and on their
potential in cancer immunotherapy. After loading with antigen, DCs exhibit the
properties of both antigen and adjuvant. Immunity or tolerance, the fine
regulation of these two distinct functions is not completely understood. Short
exposure of DCs to temperatures of 39°C or 40°C differentially increased the
secretion of interleukin (IL)-12 and decreased the secretion of IL-10 and
tumor necrosis factor (TNF), by maturing DCs. These fever-like conditions
induced a regulation of cytokine production at the single-cell level. In
addition, short-term exposed LPS-maturing DCs to 39°C induced a stronger
reaction with allogeneic CD4+ T cells than maturing DCs incubated at 37°C.
These results provide evidence that temperature regulates cytokine secretion
and DC functions. Radio frequency thermal therapies are also of great value,
in introducing localized heat. It can also be introduced by labeled antibodies
in near-infrared fluorescence reinforcement, not necessarily in detection.

DCs pulsed with tumor fragments, or tumor RNA, are all capable of eliciting a
tumor-specific cytotoxic T-cell response. Recently, several groups have
reported that hybrid cells generated by the fusion of tumor cells and DCs also
produce immunogenicity against tumor fused polyethylene glycol (PEG). An
electrofusion protocol was used to promote the fusion of tumor cells and DCs.
This approach presents practical advantages that can be applied to cells
freshly isolated from a tumor sample without any prior culturing. This also
shed light on possible ways to fuse cells electrically, in vivo.

In molecular biology study of blocking Stat3 signaling for cancer treatment,
it is discovered that in vivo gene therapy experiments introducing a
dominant-negative STAT-3ß gene into tumors demonstrated tumor regression
associated with massive intratumor inflammation and activation of systemic
tumor-specific T cell responses, even when a relatively small proportion of
the tumor cells were transduced.
This becomes interesting, when the question posted is directed to: How could
the immunologists handle tumors without known specific antigens, but still
antigenic? What are the in vivo biological elements response to RFA and other
instrumentations introducing localized cell death with different physics
principles? Given the selected target is epoxide group, what are the
biological processes generating these materials? I have a chance to work in a
group using epoxide group as response elements. Given there are ways to
fracture the cells in vivo, how could the immunology system face the scenario?
What are the good and bad aspects of physically tools to load DC with tumor
antigens in vivo, allowing clinically practical targeting? It is interesting
because “Injection of antigen loaded DCs can boost tumor-specific immunity in
patients. Studies in myeloma suggest that the use of autologous tumor as a
source of antigen may be the preferred approach. Boosting antitumor immunity
may be a useful strategy to prevent tumor progression in patients with
asymptomatic macroglobulinemia.”
The choice of focus
Two mechanisms were created—central and peripheral tolerance—both of which
are controlled and maintained by DCs. Central tolerance occurs in thymus where
newly generated T cells with a receptor that recognizes components exposed by
mature thymic DCs are deleted. However, many self-antigens may not access the
thymus while other are expressed later in life.
The nature of interaction between apoptotic and necrotic cells and DCs is
confusing. It is difficult for me to conclude whether these differences were
due to variability of antigen sources or the differences in conditions and
differentiation stages of DC generation: Only DCs pulsed with apoptotic cells,
but not necrotic cells, induced class I-restricted cytotoxic lymphocytes
(CTLs). Or, rather, DCs cannot be activated by apoptotic cell death; the
induction of DC maturation by CD 40 ligand is necessary to induce maximal
proliferation of purified CD8-T cells. Maturation also creates a dilemma of
tolerance. When DCs are capturing microbes and also maturing in response to
signals delivered through Toll-like and TNF-receptor family members, they also
capture dying self-tissues, as well as innocuous environmental proteins. How
do maturing DCs focus the immune response on the danger signals? The risk of
inducing inappropriate immune response is especially great when one considers
that DCs require very small amounts of a TCR stimulus to activate naïve T
cells. Therefore, there is a risk that the induction of immunity to pathogens
could be accompanied by the induction of immunity to self and environmental
antigens captured by the DCs.
When danger signal is introduced, it is necessary to know that DCs are
distributed everywhere, of different kinds. “DCs are located at body
surfaces, especially the skin and airways, in the interstitial spaces of many
organs, lymphoid tissues, blood, afferent lymphatic tissue, the conduits
between peripheral tissues and immunologically active LN. DCs can branch into
epithelia, by expressing important molecular components of intercellular
junctions, DCs at body surfaces may even insinuate through tight epithelia,
extending their processes into the environment to capture proteins without
breaking the epithelial barrier. In mucosal associated lymphoid tissues, DCs
lie beneath the antigen-transporting epithelia, again in the niche to capture
antigens transported through epithelial M cells.” DCs are present in normal
meninges, choroid plexus, and cerebrospinal fluid, but absent from the normal
brain parenchyma. Inflammation is accompanied by recruitment and/or
development of DCs in the affected brain tissue. DCs present in different
compartments of the CNS are likely to play a role in the defense against CNS
infections, and also may contribute to relapses/chronicity of CNS inflammation
and to break-down of tolerance to CNS autoantigens. CNS DCs can therefore be
viewed as a future therapeutic target when there are damages introduced,
within the brain. Nevertheless, prior work demonstrating the function of DCs
as inducers of primary immune responses involved adoptive immunization with
DCs cultured in vitro with antigen and then injected, or strong T cell
responses in the setting of contact allergy and transplantation. Tissue
disruption and inflammation alter DCs, increasing expression of critical
costimulators. These altered DCs are referred to as mature. The critical role
of DC maturation in immunogenicity support the notion: the immune system must
focus on antigens delivered as “danger signals”.
What confusing is how could DC differentiate various signals received and
differentiate their responses to generate tolerance from immunity, given there
is a cluster of cell death events? I do not have good answers and the
following are just direct up-liftings from literature. One method to dampen
immune function is to prepare DCs ex vivo and expose them to antigen but not
to full-maturation stimuli. These DCs, when reinfused, downregulate immunity
and can induce regulatory T cells. Experimentally, it has been necessary to
use high doses of soluble proteins and usually preprocessed peptides to induce
tolerance. It is know that for dying cell uptake, there are two pathways. The
exogenous pathway: endocytosed proteins are presented by a TAP-dependent
process, without the standard requirement for endogenous biosynthesis in the
DCs. The endogenous pathway: likely to be receptor mediated, has just become
evident with DCs in vivo. Most CD11c+ DCs in vivo are able to take up
particulates, but in the case of dying cells, only the CD8+ subset is active.
These cells include radiated self splenocytes, allogeneic cells killed by NK
cells, and tumor cells. The selective uptake by CD8+ DCs implies the existence
of a receptor pathway. At the moment, CD36 is the only candidate receptor that
is more abundant at the mRNA level in CD8+ DCs. Importantly, the uptake of
dying cells takes place continuously in the steady state, as observed directly
by injecting dying self (splenocytes) or tumor cells labeled with the stable
fluorochrome. The uptake of dying cells is followed by efficient presentation
to MHC class I- and class II-restricted T cells. Tumor-derived factors
dramatically affect DC differentiation by down regulating effective antigen
presentation. Several tumor-derived factors including vascular endothelial
growth factor (VEGF) have been implicated in abnormal DC differentiation.
Considerable evidence connects histone H1 to gene regulation. The role of this
histone in cell differentiation remains unknown. In this study, we have
investigated a possible role of H1° in differentiation of myeloid and
lymphoid cells. It was found that H1° is involved in differentiation of DC
but not macrophages, granulocytes, or lymphocytes. Tumor-derived factors
inhibit H1° expression in HPC that may contribute to defective DC
differentiation in cancer. The melanoma antigens (MAs) are, therefore,
important potential targets for immunotherapy of melanoma. However, nearly all
defined MAs are nonmutated "self" antigens expressed not only by tumors but
also by normal tissues. Whether immune recognition and functional T-cell
memory to these antigens are present in healthy individuals and melanoma
patients is therefore a central question in the immunotherapy of melanoma. The
in situ biology and function of MA-specific T cells are interesting. There is
a better work on the conceptual challenges. Steinman’s group has key interest
on how DC will react, focusing on specific antigen, in the background of
harmless epitopes. I have a tendency to figure out ways to break tolerance.
Oxidation events and antibody
Destruction of microbes within phagocytes, such as macrophages and
nutrilphils, ensues by at least three cooperative processes: production of
reactive intermediates of oxygen (ROI), and exposure to preformed polypeptide
antibiotics. Thus, despite its small invariant set of antigen receptors, the
innate immune system deploys most of the chemical processes that directly kill
pathogens. Since Ehrlich's recognition of the potential of antibodies as
therapeutic agents last century, the development of mAb technology around
1975, and advances in mAb engineering since then, mAbs have gained importance
for the treatment plans. The considerations of using in vivo antibody’s
catalytic activity in response to out field for none solid tumor treatment is
something new. I fail to realize the importance of mitochodria pathway’s
importance in introducing localized damage, because I do not think it would
have enough specificity.

Solid tumors are invariably less well oxygenated than normal tissues.
Prolonged hypoxia of the tumor tissue also leads to necrosis, and necrotic
regions are also characteristic of solid tumors. These two characteristics
(hypoxia and necrosis) represent clear differences between tumors and normal
tissues. Around solid tumors, there is usually a region of fluid with
oxidation by-products. They are potentially exploitable in cancer treatment.
For none solid tumors, they might also encounter antibody to introduce trance
oxidation events on membrane. One none solid tumor is chronic myeloid leukemia
(CML). CML responds to immune-mediated therapies.

It is a usual way to use in vivo target or to introduce adjuvant for MRI
imaging. Oxidation and nitration events at the necrosis region are some of the
targets. Macrophages and nutrilphils all introduce oxidation and nitration
materials. So does radiation. Radiation introduces oxidation of lipids. The
diffusion of those molecules might be relatively free for their chemical
properties. Antibodies, regardless of source or antigenic specificity, can
convert molecular oxygen into hydrogen peroxide, thereby potentially aligning
recognition and killing within the same molecule. This is a new chemical arm
for the immune system. Antibodies catalyze the generation of ozone by a water
oxidation pathway. The overall process is postulated to involve more than one
equivalent of the lower-energy singlet state of molecular oxygen (1O2) and to
proceed via dihydrogen trioxide (H2O3) as a key intermediate (Eq. 1).


When various free radicals interacting with lipids, there might be ways using
atomic index of specific structure (hydrogen associated with oxidation and
nitration), to introduce localized cell death. On this aspect the in vitro
study’s catalytic effect would lead to the interest of the structure study of
the catalytic pocket.
The way to control antibody production is at multiple steps. For example:
Plasma cells are terminally differentiated final effectors secreting
antibodies. Transcription factors Bcl-6 and Pax5, which are required for
germinal center B cells, block plasmacytic differentiation and repress Blimp-1
and XBP-1, respectively. The T helper lymphocyte is responsible for
orchestrating the appropriate immune response. The recognition of the
polarized T helper cell subsets Th1 and Th2 has led to an understanding of the
role of these cells in coordinating a variety of immune responses, both in
responses to pathogens and in autoimmune and allergic disease.
Macrophages and DCs play an important role in regulating B cell responses and
associated with Ab production. DCs have important roles in B-cell activation
and regulation of antibody synthesis. Rat DC makes short term interactions
with resting B cells and these interactions can be stimulated by cross-linking
molecules on cell surface. These DC can retain antigen in native form for at
least 36 h in vivo and in vitro and can subsequently release it for
recognition by B cells. In vivo antibody responses induced by antigen-pulsed
DC are skewed towards IgG. In vitro, naive B cells incubated with
antigen-pulsed DC subsequently secrete IgM and IgG when cultured with an
antigen-specific CD4+ T-cell line, whereas if B cells are incubated with
antigen without DC, only IgM is produced. Human macrophages generated in vitro
strongly co-stimulate proliferation of dense human tonsillar B cells ligated
via their B cell antigen receptor (BCR) but not proliferation via CD40.
Similarly, DCs also markedly enhance BCR-activated B cell proliferation.
Dendritic cells have many subtypes. In humans, the expression of toll-like
receptor 9 (TLR9) is restricted to B cells and plasmacytoid dendritic cells
(pDC). The pDC is characterized by the ability to rapidly synthesize large
amounts of type I IFN (IFN-alpha and IFN-beta) in response to viral infection.
In contrast to other dendritic cell subsets which express a broad profile of
TLRs, the TLR profile in PDC is restricted to TLR7 and TLR9. An intriguing
feature of PDC is its ability to simultaneously produce the two major
Th1-inducing cytokines in humans, IFN-alpha and IL-12, both at high levels.
The ratio of IFN-alpha versus IL-12 and the quantity of these cytokines are
regulated by T helper cell-mediated costimulation via CD40 ligation.
Controlling an immune response is equally complex as is its launching. Indeed,
upon entry of the pathogen, for instance, the influenza virus, DCs will
capture and present microbe-derived antigens to immune effectors to induce
immunity. However, DCs will present not only virus antigens but also
self-antigens. Thus, a mechanism must be in place to focus the reaction on
danger and not self.
Antibody function in tumor immunology is also an important part. DNA
vaccination against tissue-restricted antigens is a strategy for cancer
therapy. Immune tolerance and autoimmune of self antigens has been
considerations in mind. Immunization with xenogeneic DNA orthologues elicits
tumor immunity. One model that we have developed entails immunization of mice
against tyrosinase-related protein-2 (Tyrp2) using cDNA encoding homologous
human Tyrp2. A subset of mice immunized with human Tyrp2 developed antibody
responses to Tyrp1. This implies that the appearance of anti-Tyrp1 antibodies
was not simply a consequence of the destruction of melanocytes by T-cells
recognizing Tyrp2. To study the role of subdominant epitopes in tumor
rejection we have used EL4 tumor cells and their ovalbumin (OVA)-transfected
counterpart E.G7. Immunization of mice with irradiated EL4 cells conferred
protection against challenge with EL4 and E.G7. Surprisingly, immunization
with irradiated E.G7 cells did not protect against a subsequent challenge with
EL4 or E.G7. Lack of immunogenicity of the OVA-expressing tumor could not be
overcome by combination of a CD40 activating antibody with immunization
against E.G7 or OVA. Our results suggest that immunization against subdominant
epitopes is more effective than vaccination against dominant epitopes.
“Upon activation, the autoreactive cells may lead to autoimmunity. The need
for peripheral tolerance occurs in lymphoid organs by induction of T cell
anergy rather than deletion. The development of peripheral tolerance involves
immature DCs. These cells sitting within tissues capture the remains of cells
that die in the process of physiological tissue turnover. Because there is no
inflammation accompanying this process, the DCs remain immature and migrate
toward the draining lymph nodes. These immature DCs, which lack co-stimulatory
molecules, present the tissue antigens to autoreactive T cells, which in the
absence of co-stimulation; enter into a state of anergy. Hence, increased
availability of mature DCs may result in autoimmunity. Thus, we now view SLE
as a disease where IFN-induced DCs phagocytose cell nuclei that circulate in
the blood of these patients and its components are presented to autoreactive T
cells and B cells, leading to the generation of anti-nuclear antibodies
including anti-double-stranded DNA antibodies. What we learn from studying
autoimmunity will help us induce strong tumor-specific immunity.”
Diffusion and fractional diffusion model for breaking tolerance
“What is the source of extracellular HSPs in vivo? What is the physiological
significance of HSPs in the immune response, in the context of stress
responses and microenvironment of cancers?” Answers to these questions have
obvious implications both in terms of understanding the immune system but also
in clinical translation of HSP technology for cancer immunotherapy. In order
to solve the prediction problem of breaking tolerance, fractional diffusion
model is important to be introduced. Under the condition of stress or
"danger," HSPs are not only increased in expression level (for the purpose of
cytoprotection and antigen presentation) but could also undergo dynamic
redistribution to gain access to the extracellular environment. Although the
cell biological basis of extracellular distribution of HSPs is unclear, both
the induction of HSPs and their cell surface expression or secretion might
conceivably contribute to sending an "ON" signal to activate the immune system
and hence to break down peripheral tolerance.

Introducing fractional diffusion factor in reaction diffusion model in
prediction program helps to understand interactions between free diffusion
factors and migration factors. This is useful not only in neuronal signaling
dynamics, but also has application in pharmacologically manipulating systems.
One example is gp 96 within, on the surface of various compartments (ER, Golgi
and cell surface), and out of tumor cells in different states, different
cellular compartments, introducing to the cellular environments and their
interactions with immunology players and those players’ consequent behavior.
In the mean time, signaling factors’ interaction with migrating cells as
melanocytes can also be interpreted, by this model, meaningful in melanoma
development anticipation. Melanoma has been the most widely studied cancer
with regard to tumor immunity. There is no direct evidence that melanoma is
more immunogenic than other tumors. Melanomas have been observed to undergo
spontaneous regression with higher frequency than most other types of cancer.
However, because melanomas are pigmented, primary tumors arise and metastases
happen cutaneously. They are therefore easy to observe.
Diagramming Networks
Regulatory signals governing melanoma genesis may originate from the
surrounding host cells, either directly through physical contact or indirectly
through soluble factors and extracellular matrix molecules in a precise
spatiotemporal order. One consideration is that melanocytic transformation may
be unleashed by defects in communication pathways maintaining tissue
homeostasis. The other consideration is a neglect of immune surveillance
system to this action. Traditional way to study protein-protein interactions
is blotting. Kinetic models are involved. Protein array is developing in
phosphorylation events, and protein-protein interactions without additional
labeling steps of probe proteins. Several strategies have been employed to
construct protein chips that retain the structural integrity and functional
activity of the arrayed proteins. Polyacryl-amide gel pads have been used to
absorb protein samples, but require manufactured masks and electro-phoresis to
accelerate diffusion of molecules. Glass slides derivatized with aldehyde
groups or activated bovine serum albumin to attach proteins or use HisX6 tags
to attach protein to nickel-coated slides. Another important consideration in
the development of protein chips is the method of detection. It was
accomplished with probes that were labeled with fluorescent dyes, traditional
enzyme-linked immunosorbent assay (ELISA) techniques and fusion with red and
green fluorescent proteins. With other proteomic technologies, there is an
enormous effort in pre-industrial research to define the identities,
quantities, structures and functions of complete complements of proteins and
to characterize how these properties vary in different cellular contexts. With
the development of computational facilities, simulation machinery is looking
into combining classical electrodynamics with relativity to understand quantum
mechanics. The joint effort of tumor treatment requires close cooperation
between laboratories, bridging experimental, clinical, industrial research and
advocacy groups. The substantive hurdles to rejecting established tumors
suggest that immunotherapies will need to stimulate broad and sustained host
responses. Unfortunately, these same requirements also imply that tumors may
accomplish immune escape by devising strategies that undermine diverse immune
mechanisms. The combination of immunotherapies and other treatments including
blocking resistance pathways and physical therapies may be worth exploring.
Conclusion:
It is interesting to look into immunology events associated with localized
cell death introduction in a model system. It is known that oxidation events
around solid tumors could be used. It seems that for none solid tumors,
antibody could introduce localized oxidation events to lipid membrane. Certain
atomic index could be the target of electric magnetic field. The physics basis
supporting this method is a going on project. Immunology events are
interesting, because they introduce specific targets and they introduce ways
to solve aftermaths.

1 HADRONIC JOURNAL VOLUME 23, NUMBER 5, October 2000
UNIFICATION OF FORCES ACCORDING TO RELATIVITY FOR ROTATIONS, 487
EXPERIMENTAL VERIFICATION OF RELATIVITY FOR ROTATIONS , 551
2 Dr. Yu has not got her paper published, by now. I used Drew Pardoll’s rumor
transferring. Interestingly, there are other observations that small amount of
tumor damage events will lead to amplified tumor clearance. The problem is
that the result is not always stable and the effect is not always there.
3 I do not really understand the internalization methods.




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※ 修改:·justacode 於 Jun 4 18:44:27 修改本文·[FROM: 140.251.]
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