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 Last week I mentioned that the current chemical assault being used by traditional medicine is CLEARLY not the answer. Many were interested in what my treatment for hepatitis C involves as. This is especially evident after reviewing the articles on hepatitis C posted in this week’s newsletter.

My approach for hepatitis C involves first and foremost making sure there is rigid compliance to the dietary recommendations listed in Read This First.

Once that is implemented one need to minimize other toxic influences to the immune system. Amalgam fillings are typically present and need to be removed along with a comprehensive mercury detoxification program by a competent clinician.  Elimination of toxic deposits in the body, especially pesticides through sauna detoxification is another helpful approach. 

However, I believe the critical element involves normalizing the autonomic nervous system by uncoupling the emotional traumas and conflict that typically seem to impair its optimal functioning. Applied Psycho Neurobiology is the current strategy I am using.

The following article also supports the hepatitis theory described above:

Hepatitis C virus (HCV) specific sequences are demonstrable in the DNA fraction of peripheral blood mononuclear cells from healthy, anti-HCV antibody-negative individuals and cell lines of human origin.  By Dennin RH, Chen Z

No convincing support has been provided so far for the existence of extrahepatic hepatitis C virus particles that should correspond to the sometimes extremely high concentration of ‘HCV-RNA’ in serum or plasma. If a naturally occurring HCV-specific DNA were to be found, a concept for at least some phenomena in terms of the pathophysiology of HCV should become conceivable.

DNA was extracted from peripheral blood mononuclear cells of eleven healthy, anti-HCV-negative individuals, including five long term blood donors, and cells from different cell lines. DNA was subjected to nested polymerase chain reaction omitting a reverse transcriptase step with primers of the 5’NC as well as part of the core region of HCV.

Direct polymerase chain reaction, i.e. without a reverse transcriptase step, revealed HCV-specific sequences in the DNA fraction of peripheral blood mononuclear cells of different origin: healthy anti-HCV negative individuals, furthermore in HeLa and MT2 cells.

The fragments found were of expected length as well as of shorter and of longer than expected length with respect to the sequence of the HCV genome framed by the primers applied.

The results derived from additional hybridization, restriction endonuclase analysis, and sequencing demonstrated HCV-specific sequences in the expected fragments with both a high degree of homology and deletions, respectively, substitutions, as compared to a prototype strain.

However, the longer than expected fragments also contained sequences not specific for HCV.

DURHAM, N.C. — A research team from Duke Health has developed an antibody from the body’s own immune system that preferentially attacks cancer cells. Own Immune System attacking cancer …

Source: Antibody appears to attack cancer cells, leaving other cells unscathed by Duke University Med Center

DURHAM, N.C. — A research team from Duke Health has developed an antibody from the body’s own immune system that preferentially attacks cancer cells.

Own Immune System attacking cancer cells

The antibody works by targeting a natural defense mechanism that cancer tumors exploit.

Cells in the body essentially use a home security system that relies on certain proteins to protect the cell surface and keep it safe. These proteins help the cell avoid injury and even death from unwanted activation of the immune system.

In a paper published online May 5, 2016 in Cell Reports, the Duke team describes the workings of a cancer-fighting antibody they discovered, developed and tested in cell lines and animal models. The antibody dismantles a specific part of a cancer cell’s defense system and then employs several mechanisms of attack.

“This is the first completely human-derived antibody developed as an anti-cancer therapy, which is very different from other immunotherapy approaches,” said senior author Edward F. Patz, Jr., M.D., the James and Alice Chen Professor of Radiology and professor in the Department of Pharmacology and Cancer Biology at Duke.

Patz and colleagues — including principals from the Duke Human Vaccine Institute who have been advancing the development of antibodies for an HIV vaccine — started with the observation that some lung cancer patients have early-stage tumors that never progress to advanced disease.

Antibodies against a protein called complement factor H, or CFH

One of the features that separated these patients from those who had more lethal tumors was the presence of antibodies against a protein called complement factor H, or CFH, which protects cells from an immune system attack.

CFH works by preventing activation of an important immune response. It inhibits the deposit of a complement C3b protein on the cell surface. Complement C3b initiates the degradation of the cell membrane, which eventually leads to cell death.

Once the antibody for CFH was identified, Patz and colleagues sought to explore how this immune response could be optimized as a cancer therapy. Critical to that effort was finding a way to produce antibodies that recognized the exact same part of CFH as the autoantibodies made by the early-stage cancer patients, thus assuring that the antibodies would have a particular affinity for cancer cells.

White blood cells from CFH antibody-producing cancer patients

Patz and colleagues pooled the white blood cells from CFH antibody-producing cancer patients and then isolated and cloned the antibody genes from single immune cells that make the specific antibodies.

This was an efficient process that enabled the researchers to produce mature antibodies that recognized the same region of CFH targeted by the original patient’s immune systems — therefore leading to the attack of cancer cells, not healthy cells.

The researchers then tested the antibodies in multiple cancer cell lines, including lung, gastric and breast cancers in lab dishes, and in tumors in living mice. They found that the antibodies caused tumor cell death without any obvious side effects. The antibodies also appeared to trigger an additional adaptive immune response when the damaged cells sent signals to recruit an army of lymphocytes, creating a potentially more lethal systemic attack.

“We believe it might be this additional cellular response that could potentially have the most profound impact on cancer outcomes long-term,” Patz said, noting that further tests would be required to understand the full potential of the approach.

“This could represent a whole new approach to treating cancer, and it’s exciting because the antibody selectively kills tumor cells, so we don’t have significant side effects to achieve tumor control,” Patz said. “We believe we can modulate the immune response and let the body’s own immune system take over to either kill the tumor or keep it from growing.”

Adverse Reactions from Cancer Meds

Limitation of calorie intake by 20-30% compared to usual intake was found to significantly extend the life of rodents, yeast, C. elegans, D. melanogaster, and potentially primates . In mammals, suc…

Source: Live longer by cutting calorie intake by 20-30%

Limitation of calorie intake by 20-30% compared to usual intake was found to significantly extend the life of rodents, yeast, C. elegans, D. melanogaster, and potentially primates . In mammals, such a diet was also found to lower the risk of obesity, cardiovascular disease, cancer, inflammation, and neurodegenerative diseases (shown in 1 and 2).

The mechanisms by which caloric restriction (CR) exerts its health-promoting effect are multiple and include modifications of the epigenome. For example:

A reduction in calories attenuates age-associated changes in the expression of DNMTs, increases the activity of HDAC and affects the expression of various miRNAs.

It also changes the gene methylation profile, e.g. HRAS and reduces the MYC hypomethylation observed in aging mice. RNA-seq data from the rat cerebral cortex showed that miR-98-3p (overexpressed during CR) alters HDAC and HAT activities .

The best established link between CR and epigenetic modifications is represented by sirtuins. Amongst the seven mammalian sirtuins, the most studied within the context of aging are SIRT1, SIRT3 and SIRT 6. The expression of sirtuins increases during CR and is associated with prolonged lifespan in model organisms. This effect is confirmed by the lack of CR-associated lifespan extension in the absence of these proteins.

 The newest data has suggested that a restriction of only 10% might be enough to delay/prevent a number of age-related diseases.

The role of sirtuins in CR seems to be crucial due to their interaction with a variety of proteins such as PGC-1α, p53, LXR, FOXO family and NF-κB. The deacetylation of FOXO increases downstream gene expression. Whilst, the deacetylation of NF-κB results in the inhibition of its pro-inflammatory action.

 In summary, CR is, so far, the only intervention with well proven beneficial effect on healthspan and lifespan. Fortunately for us, the newest data has suggested that a restriction of only 10% might be enough to delay/prevent a number of age-related diseases or to alleviate their course. However, a 20-30% restriction might be necessary to extend the length of life.

While the interim results from the Starbeam study are early, with only three of the 17 patients having completed the study thus far, we are pleased to see evidence of neurologic and radiographic stabilization of CALD,” said David Davidson, M.D., chief medical officer, bluebird bio. “All patients are free of MFDs and most have had no progression in NFS. Brain MRI is the primary tool to quantify disease activity, and it is encouraging that most patients in the study have had stabilization of Loes score and resolution of gadolinium enhancement. We look forward to sharing additional data from this trial as the results mature, and would like to express our gratitude to the study investigators, and especially to the patients and families who are participating in this trial.”

David Williams receives research support from bluebird bio for research related to sickle cell disease, and the company has licensed intellectual property from Boston Children’s Hospital for technology related to gene therapy for hemoglobinopathies that Williams co-invented.

About the Starbeam (ALD-102) Study

The Starbeam Study is assessing the efficacy and safety of an investigational gene therapy in boys up to 17 years of age with CALD. It involves transplantation with a patient’s own stem cells, which are modified to contain a functioning copy of the ABCD1 gene. This gene addition should result in the production of functional adrenoleukodystrophy protein (ALDP), a protein critical for the breakdown of very long chain fatty acids (VLCFAs). Buildup of VLCFAs in the central nervous system contributes to neurodegeneration in CALD.

Subjects enrolled in the study are:

• Eligible for allogeneic hematopoietic stem cell transplant (HCT) but with no matched sibling donor
• Confirmed early-stage, active CALD as indicated by gadolinium enhancement on MRI
• Have a Loes score between 0.5 – 9.0
• Have an NFS of one or less

About CALD

Also known as Lorenzo’s Oil disease, cerebral adrenoleukodystrophy (CALD) is a rare and fatal, X-linked, inherited, neurodegenerative disease that primarily affects young boys. CALD involves a progressive destruction of myelin, the protective sheath of the nerve cells in the brain that are responsible for thinking and muscle control. Symptoms usually occur in early childhood and progress rapidly if untreated, leading to severe loss of neurological function and eventual death. In boys affected by CALD, learning and behavioral problems are often observed in mid-childhood between the ages of 3 and 15 years (median age 7). The worldwide incidence rate for ALD is approximately one in 21,000 male newborns; of those, 30-40 percent are affected by CALD, the cerebral form of the disease.

Currently, the only effective treatment option for patients with CALD is allogeneic HCT. Complications of allogeneic HCT include a significant risk of treatment-related mortality, graft failure, graft-versus-host disease (GvHD) and opportunistic infections, particularly in patients who undergo allogeneic HCT and do not have a matched sibling donor.

Researchers with the UC Davis Comprehensive Cancer Center, MIND Institute identify more than 40 common genes.   Autism and cancer share more than 40 risk genes, suggesting that common mechanisms underlying the functions of some of these genes could conceivably be leveraged to develop therapies not just for cancer but for autism as well, an extensive assessment by researchers with the UC Davis MIND Institute and Comprehensive Cancer Center has found.

The authors identified 43 specific genes with autism susceptibility that also have an association with cancer.

“This striking coincidence of a remarkably large number of genes implicated in both autism spectrum disorder and cancers has not been previously highlighted in the scientific literature,” said Jacqueline Crawley, MIND Institute distinguished professor and endowed chair. “Potentially common biological mechanisms suggest that it may be possible to repurpose drug treatments for cancer as potential therapeutics for neurodevelopmental disorders.”

“Autism and Cancer Shared Risk Genes, Pathways and Drug Targets,” is published online in Trends in Genetics, a Cell Symposia publication. Crawley collaborated on the work with professor and chair of the UC Davis Department of Microbiology and Molecular Genetics Wolf-Dietrich Heyer, who is affiliated with the Cancer Center and Janine LaSalle, professor of medical microbiology and immunology, who is associated with the MIND Institute.

“Autisms” are best conceptualized like cancers, the authors write: in the plural. Like cancers, the behaviorally defined condition encompasses a broad range of putative causes, symptoms and outcomes.

Included in the dozens of genes implicated in both cancer and autism are genes for relatively rare syndromes, such as Rett syndrome and tuberous sclerosis, whose sufferers experience an array of physical and neurological symptoms, including intellectual disability, as well as communication deficits characterized as autism.

What does tumor cell proliferation have in common with synapse formation and brain development?

“Errors associated with genome maintenance during fetal life may occur at critical time periods for [brain development] resulting in neurodevelopmental disorders,” said Heyer, “whereas errors more commonly occur during adult life in cell types susceptible to tumors.”

“Genes encoding nuclear proteins involved in epigenetic functions were frequently shared between cancer and ASD, implicating the importance of aberrant gene regulation in both disease states,” La Salle said.

Considerable translational value can be gained from a new focus on understanding the genetic commonalities of autisms and cancers.

“It may be possible to repurpose available cancer drugs with reasonable safety profiles as targeted treatments for ASD,” the authors write. “Stratifying individuals with ASD who harbor a risk gene for autism that is also a risk gene for cancer may enable therapeutic development of personalized medicines based on the specific causal mutation.”

The concept for their Forum piece in Trends in Genetics grew out of a Cancer Research Symposium at UC Davis in 2014 “Common Themes and Mechanisms in Cancer and Neurodevelopmental Disorders.” Organized by Ralph de Vere White, director of the UC Davis Comprehensive Cancer Center, and Leonard Abbeduto, director of the UC Davis MIND Institute, the interdisciplinary symposium sparked discussions between Heyer, LaSalle and Crawley, demonstrating the strongly collaborative interactions of UC Davis faculty across disciplines.

Latest update on Clinton campaign funds For months, you’ve heard the Clinton campaign endlessly repeat in interviews and on social media that they have raised millions and millions of dollars…

Source: Elizabeth Warren and Bernie Sanders are for our future

You need a builder for this circular homes, delivered from the East Coast factory, and need inside panels. For more info , email motherhealth@gmail.com

Source: $25k for 500 sq ft home, modular panels

You need a builder for this circular homes, delivered from the East Coast factory, and need inside panels. For more info , email motherhealth@gmail.com

Infections continue to threaten human health. With remarkable genetic flexibility, pathogenic organisms outsmart available therapies. Fortunately, microbial versatility is matched by the host immune system, which evolves in dialogue with the microbes. Therapies that enhance the beneficial effects of the immune response represent a promising, but under-explored, therapeutic alternative to antibiotics.

A recently published paper identifies a new therapeutic target for the treatment of bacterial infections that regulates the immune response. Researchers at Lund University in Sweden have now found an “off” switch for destructive inflammation in infected kidneys that does not impair the anti-bacterial defense.

The challenge is to strengthen the good, antibacterial defence without causing tissue damage. Inflammation accompanies most infections and symptoms like fever and pain are the price to pay for an effective defense.

”Here we address how to avoid the exaggerated immune response to severe infections, which can lead to tissue destruction and even organ failure” says Manoj Puthia, researcher at Lund University, Sweden and lead author of the study.

”We knew that specific transcription factors regulate innate immune responses to bacterial infection and that the outcome of infection be beneficial or destructive, depending on how these regulators work” says Professor Catharina Svanborg. ”We have also identified genetic variants in susceptible patients that support this concept. ”

Using mice lacking the closely related transcription factors IRF-3 or IRF-7, we were surprised to find that IRF-3 and IRF-7 control different facets of the immune response to kidney infection and that this determines the susceptibility to acute pyelonephritis, which is a severe, potentially life-threatening bacterial infection of the urinary tract.

In contrast to mice lacking IRF-3, which became very ill, Irf7-/- mice were protected from infection and chronic inflammation, suggesting that suppression of Irf7 might be beneficial.

”Based on these findings identifying Irf7 as an immunotherapeutic target, we used siRNA therapy to silence Irf7 and were able to demonstrate protection in susceptible mice,” says Dr. Puthia.

Infections remain the major cause of the deaths worldwide, especially in developing and poorly developed areas. While antibiotics have greatly reduced illness and mortality, many pathogens have developed resistance and we are facing a global crisis.

“We propose to fight infections by learning from the innate immune system. We also need to define why the immune system is not protecting certain patients and learn to replenish these defects by boosting the ”good” immune response.”

 After a stroke

After a stroke, there is inflammation in the damaged part of the brain. Until now, the inflammation has been seen as a negative consequence that needs to be abolished as soon as possible. But, as it turns out, there are also some positive sides to the inflammation, and it can actually help the brain to self-repair.

“This is in total contrast to our previous beliefs”, says Professor Zaal Kokaia from Lund University in Sweden.

Zaal Kokaia, together with Professor of Neurology Olle Lindvall, runs a research group at the Lund Stem Cell Center that, in collaboration with colleagues at the Weizmann Institute in Israel, is responsible for these findings. Hopefully, these new data will lead to new ways of treating stroke in the future. The study was recently published in the international Journal of Neuroscience.

When stroke occurs, the nerve cells in the damaged area of the brain die, causing an inflammation that attracts cells from the immune system. Among them you find monocytes – a type of white blood cells produced in the bone marrow.

The monocytes travel to the inflamed area, and here they develop into macrophages that clear out any dead tissue. But this is not all that they do: they also secrete substances that help the brain repair the damage.

“This is what we, together with Michal Schwartz’s research group in Israel, have been able to show”, says Zaal Kokaia.

Most stroke patients recover at least partly over time. This spontaneous improvement is well known, but not its exact cause. The Lund researchers now believe that the improvement is partly due to the substances released by the immune cells.

In their study, they actually performed the opposite: in animal model of stroke they were able to ablate monocytes from the blood. Mice with decreased number of circulating monocytes were much less successful in their recovery from stroke than mice whose immune system was functioning as normal.

Today’s treatment against stroke primarily involves dissolving or removing the blood clot that caused the stroke. However, such treatments must be performed in the very early phase after the insult, which means that most stroke patients are too late to receive it. A future treatment method – one that could be based on the Lund researchers’ new findings and that aims to promote self-healing – could be implemented later. This treatment could start at some point within the first few weeks, rather than within the first few hours after a stroke.

The Lund researchers have focused on what happens in the brain during this later stage. Among other things, they were the first to show that, after a stroke, the brain produces new nerve cells from its own stem cells. They now want to proceed with animal experiments to see if the self-healing can be improved by adding more monocytes to the brain, or by stimulating the production of monocytes in bone marrow.

“Obviously, there is a difference between mice and humans, but there is no indication that our brains function differently in this regard”, says Olle Lindvall.

He further argues that this new insight concerning the positive effects of inflammation could also be applied to other diseases. The Lund research group’s collaborators from Israel have obtained similar results in cases of spinal cord injury.

http://medicalxpress.com/news/2016-04-immune-cells-brain-self-heal.html

Important points in the development of Alzheimer’s disease: sugar intake [ pancreas health] NSAID intake – acidic meds vs alkaline environment for glial cells health iron, blood homeost…

Source: Alzheimer’s disease, the police cells – microglia and vasoactive intestinal peptide

Important points in the development of Alzheimer’s disease:

• sugar intake [ pancreas health]

• NSAID intake – acidic meds vs alkaline environment for glial cells health

• iron, blood homeostasis – blood vessels health from embryo to adulthood

• stress – brain/body cannot detox [ parathyroid health]

• lack of sleep – brain cannot detox [ pituitary gland health]

• bacteria in the gut – travelling to the brain [microbiome]

• prenatal development and nutrients in the womb

• glial cells – police in the brain

• vasoactive intestinal peptide – police in the gut

Summarized by:

Connie Dello Buono

About Vasoactive intestinal peptide (VIP)

Vasoactive intestinal peptide also known as the vasoactive intestinal polypeptide or VIP is a peptide hormone containing 28 amino acid residues. VIP is a neuropeptide that belongs to a glucagon/secretin superfamily, the ligand of class II G protein-coupled receptors.^[1] VIP is produced in many tissues of vertebrates including the gut, pancreas, and suprachiasmatic nuclei of the hypothalamus in the brain.^[2][3] VIP stimulates contractility in the heart, causes vasodilation, increases glycogenolysis, lowers arterial blood pressure and relaxes the smooth muscle of trachea, stomach and gall bladder. In humans, the vasoactive intestinal peptide is encoded by the VIP gene.^[4]

VIP has a half-life (t_½) in the blood of about two minutes.

Function[edit]

VIP has an effect on several tissues:

• With respect to the digestive system, VIP seems to induce smooth muscle relaxation (lower esophageal sphincter, stomach, gallbladder), stimulate secretion of water into pancreatic juice and bile, and cause inhibition of gastric acid secretion and absorption from the intestinal lumen.^[5] Its role in the intestine is to greatly stimulate secretion of water and electrolytes,^[6] as well as relaxation of enteric smooth muscle, dilating peripheral blood vessels, stimulating pancreatic bicarbonate secretion, and inhibiting gastrin-stimulated gastric acid secretion. These effects work together to increase motility.^[7]
• It also has the function of stimulating pepsinogen secretion by chief cells.^[8]
• It is also found in the brain and some autonomic nerves. One region of the brain includes a specific area of the suprachiasmatic nuclei (SCN), the location of the ‘master circadian pacemaker’. The SCN coordinates daily timekeeping in the body and VIP plays a key role in communication between individual brain cells within this region. Further, VIP is also involved in synchronising the timing of SCN function with the environmental light-dark cycle. Combined, these roles in the SCN make VIP a crucial component of the mammalian circadian timekeeping machinery.
• VIP helps to regulate prolactin secretion;^[9] it stimulates prolactin release in the domestic turkey.
• It is also found in the heart and has significant effects on the cardiovascular system. It causes coronary vasodilation^[5] as well as having a positive inotropic and chronotropic effect. Research is being performed to see if it may have a beneficial role in the treatment of heart failure.
• VIP provokes vaginal lubrication in normal women, doubling the total volume of lubrication produced.^[10]
• The growth-hormone-releasing hormone (GH-RH) is a member of the VIP family and stimulates Growth Hormone secretion in the anterior pituitary gland.

Pathology[edit]

VIP is overproduced in VIPoma.^[5] Can be associated with Multiple Endocrine Neoplasia Type 1 (Pituitary, parathyroid and pancreatic tumors). Symptoms are typically:

• Profuse non-bloody/non-mucoid diarrhea (3L+) causing dehydration and the associated electrolyte disturbances such as hypokalemia and metabolic acidosis.
• Lethargy and exhaustion may ensuey health