Tesla_WTC_Solution
6th January 2013, 20:36
http://ncsdconnection.com/main/wp-content/uploads/Hepatitis-A-B-Vaccine1.jpg
I wanted to take a moment and ask some Avalon people what they thought about a rather unpopular idea --
....................................................................................................
What do you think about this theory?
"A vaccine can disrupt
the chemical balance of your body
by simply causing your immune system
to start disliking your own cell surface proteins!"
_____________________________________________________________
The most important and poorly understood surface protein is Heparan Sulfate.
http://upload.wikimedia.org/wikipedia/commons/thumb/4/40/Heparan_sulfate.png/440px-Heparan_sulfate.png
Heparan sulfate (HS) is a linear polysaccharide found in all animal tissues. It occurs as a proteoglycan (HSPG) in which two or three HS chains are attached in close proximity to cell surface or extracellular matrix proteins.[1][2] It is in this form that HS binds to a variety of protein ligands and regulates a wide variety of biological activities, including developmental processes, angiogenesis, blood coagulation and tumour metastasis. HS has been shown to serve as cellular receptor for a number of viruses including the respiratory syncytial virus (Hallak et al. 2000)
What does Heparan Sulfate DO in the Hep B vaccine and is it understood?
http://www.ncbi.nlm.nih.gov/pubmed/18046710
Hepatology. 2007 Dec;46(6):1759-68.
Hepatitis B virus infection initiates with a large surface protein-dependent binding to heparan sulfate proteoglycans.
Schulze A, Gripon P, Urban S.
Source
Department of Molecular Virology, Otto-Meyerhof-Zentrum (OMZ), University of Heidelberg, Heidelberg, Germany.
Abstract
Contrary to many other viruses, the initial steps of the hepatitis B virus (HBV) infection, including attachment to hepatocytes, specific receptor interactions, and membrane fusion, are unsolved.
HBV infection requires the initial attachment to the carbohydrate side chains of hepatocyte-associated heparan sulfate proteoglycans as attachment receptors. This interaction initializes the multistep entry process of HBV and cannot be bypassed by alternative routes..
PROTEIN LOSING ENTEROPATHY and the plague of GUT DISEASE
http://emedicine.medscape.com/article/931647-overview
Protein-losing enteropathy (PLE) is not a single disease but a symptom. While it occurs in multiple conditions through various pathophysiologic processes, the end result is the loss of serum proteins into the GI tract. Although enteropathy is defined as an intestinal disease, and is commonly associated with the small bowel, protein-losing enteropathy includes loss of protein from the colon, stomach, and, rarely, the esophagus. Some authors have used the term protein-losing gastroenteropathy. While there is nothing unique about protein-losing enteropathy in children, the prevalence of various etiologies is different in children from that in adults.
Protein-losing enteropathy can be either a primary manifestation or a subclinical component of various diseases. Historically, patients with hypoalbuminemia of unknown cause were referred to as having idiopathic hypoproteinemia, edema disease, or nephrosis without nephrosis. These patients had neither a decrease in the production of albumin (ie, no signs of malnutrition or hepatic disease) nor an increase in albumin losses from the respiratory tract, kidneys, or skin.
In 1949, Albright et al demonstrated an increase in protein turnover in patients with protein-losing enteropathy. In 1958, Citrin et al were the first to use radiolabeled tracers to demonstrate the actual loss of a protein-containing fluid into the GI tract. Several additional diagnostic techniques using radiolabeled substrates were developed, but a major advance was made when Crossley and Elliot demonstrated that measurement of alpha1-antitrypsin (A1-AT) levels in the stool was a reliable and simple test for protein-losing enteropathy. This approach has identified various conditions that have subclinical protein-losing enteropathy as a component of the disease process.
http://www.jbc.org/content/281/12/7809.full.pdf
Protein Losing Enteropathy Seen in Vitro with Heparan Sulfate
Heparan Sulfate Plays a Central Role in a Dynamic in Vitro
Model of Protein-losing Enteropathy
*
Received for publication, September 30, 2005, and in revised form, December 19, 2005 Published, JBC Papers in Press, January 24, 2006, DOI 10.1074/jbc.M510722200
Lars Bode
Simon Murch
and Hudson H. Freeze
From the
Burnham Institute for Medical Research, Glycobiology and Carbohydrate Chemistry Program, La Jolla, California 92037
and
§
Warwick Medical School, Clinical Sciences Research Institute, Coventry CV2 2DX, United Kingdom
Protein-losing enteropathy (PLE), the loss of plasma proteins
through the intestine, is a symptom in ostensibly unrelated diseases.
Emerging commonalities indicate that genetic insufficiencies predispose for PLE and environmental insults, e.g. viral infections and
inflammation, trigger PLE onset. The specific loss of heparan sulfate (HS) from the basolateral surface of intestinal epithelial cells
only during episodes of PLE suggests a possible mechanistic link.
In
the first tissue culture model of PLE using a monolayer of intestinal
epithelial HT29 cells, we proved that HS loss directly causes protein
leakage and amplifies the effects of the proinflammatory cytokine
tumor necrosis factor (TNF). Here, we extend our in vitro model
to assess the individual and combined effects of HS loss, interferon (IFN), TNF, and increased pressure, and find that HS
plays a central role in the patho-mechanisms underlying PLE.
Increased pressure, mimicking venous hypertension seen in postFontan PLE patients, substantially increased protein leakage, but
HS loss, IFN, or TNF alone had only minor effects. However,
IFN up-regulated TNFR1 expression and amplified TNF-induced protein leakage. IFN and TNF compromised the integrity
of the HT29 monolayer and made it more susceptible to increased
pressure. HS loss itself compromises the integrity of the monolayer,
amplifying the effects of pressure, but also amplifies the effects of
both cytokines.
In the absence of HS a combination of increased
pressure, IFN, and TNF caused maximum protein leakage. Soluble heparin fully compensated for HS loss, providing a reasonable
explanation for patient favorable response to heparin therapy.
http://drugline.org/img/ail/125_126_2.jpg
Protein-losing enteropathy is an abnormal loss of protein from the digestive tract or the inability of the digestive tract to absorb proteins.
Causes
There are many causes of protein-losing enteropathy. Any condition that causes serious inflammation in the intestines can lead to protein loss. Some of the more common causes are:
celiac disease
Crohn's disease
Lymphoma
MUST READ: AUTISM TRIGGER OF GUT DISEASE CAUSED BY SHOTS
REAL MEDICAL JOURNAL!!! GLUTEN INTOLERANCE CAUSED BY HEP B
http://hepatmon.com/?page=article&article_id=387
Bacteria or parasite infection Are Hepatitis B Virus and Celiac Disease Linked?
Salvatore Leonardi
Department of Pediatrics, University of Catania, Catania, Italy
Mario La Rosa
Department of Pediatrics, University of Catania, Catania, Italy
Correspondence:
Salvatore Leonardi MD
Affiliation: Department of Pediatrics, University of Catania
City, Province: Catania,
Country: Italy
Tel: +39 095 378 2764
Fax: +39 095 378 2764
E-mail: leonardi@unict.it
Background and Aims: It has been hypothesized that nonintestinal inflammatory diseases such as hepatitis B virus (HBV) and hepatitis C virus (HCV) may trigger immunologic gluten intolerance in susceptible people. This hypothesis suggests a possible epidemiological link between these two diseases, although this assumption is still a matter of debate.
Methods: We conducted a retrospective study to assess the prevalence of celiac disease in HBV carrier patients who had been infected in childhood.
Results: None of the HBV carrier patients had immunoglobulin A antiendomysium and immunoglobulin A anti-tissue transglutaminase, but 6 patients and 1 recovered subject had immunoglobulin A antigliadin and/or immunoglobulin G antigliadin. Moreover, no patient treated with interferon therapy showed any serological marker of celiac disease.
Conclusions: Due to the small sample size, we cannot claim that there is no association between celiac disease (CD) and HBV, although in our study we did not find any CD patients. A sample size that is more representative of the prevalence of CD in Italy would better support the establishment of any possible connection between CD and HBV.
Keywords: Hepatitis B Virus;Celiac Disease;Enteropathy
__________________________________________________________
If you care about kids and adults who suffer greatly from autism spectrum disorder, please read and try to understand the post above! God Bless you for the great work.
SMART KIDS HAVE SEVERE ALLERGIES
BECAUSE OF THE MAMMALIAN HUMORAL RESPONSE
http://img145.imageshack.us/img145/4296/gifted.png
I wanted to take a moment and ask some Avalon people what they thought about a rather unpopular idea --
....................................................................................................
What do you think about this theory?
"A vaccine can disrupt
the chemical balance of your body
by simply causing your immune system
to start disliking your own cell surface proteins!"
_____________________________________________________________
The most important and poorly understood surface protein is Heparan Sulfate.
http://upload.wikimedia.org/wikipedia/commons/thumb/4/40/Heparan_sulfate.png/440px-Heparan_sulfate.png
Heparan sulfate (HS) is a linear polysaccharide found in all animal tissues. It occurs as a proteoglycan (HSPG) in which two or three HS chains are attached in close proximity to cell surface or extracellular matrix proteins.[1][2] It is in this form that HS binds to a variety of protein ligands and regulates a wide variety of biological activities, including developmental processes, angiogenesis, blood coagulation and tumour metastasis. HS has been shown to serve as cellular receptor for a number of viruses including the respiratory syncytial virus (Hallak et al. 2000)
What does Heparan Sulfate DO in the Hep B vaccine and is it understood?
http://www.ncbi.nlm.nih.gov/pubmed/18046710
Hepatology. 2007 Dec;46(6):1759-68.
Hepatitis B virus infection initiates with a large surface protein-dependent binding to heparan sulfate proteoglycans.
Schulze A, Gripon P, Urban S.
Source
Department of Molecular Virology, Otto-Meyerhof-Zentrum (OMZ), University of Heidelberg, Heidelberg, Germany.
Abstract
Contrary to many other viruses, the initial steps of the hepatitis B virus (HBV) infection, including attachment to hepatocytes, specific receptor interactions, and membrane fusion, are unsolved.
HBV infection requires the initial attachment to the carbohydrate side chains of hepatocyte-associated heparan sulfate proteoglycans as attachment receptors. This interaction initializes the multistep entry process of HBV and cannot be bypassed by alternative routes..
PROTEIN LOSING ENTEROPATHY and the plague of GUT DISEASE
http://emedicine.medscape.com/article/931647-overview
Protein-losing enteropathy (PLE) is not a single disease but a symptom. While it occurs in multiple conditions through various pathophysiologic processes, the end result is the loss of serum proteins into the GI tract. Although enteropathy is defined as an intestinal disease, and is commonly associated with the small bowel, protein-losing enteropathy includes loss of protein from the colon, stomach, and, rarely, the esophagus. Some authors have used the term protein-losing gastroenteropathy. While there is nothing unique about protein-losing enteropathy in children, the prevalence of various etiologies is different in children from that in adults.
Protein-losing enteropathy can be either a primary manifestation or a subclinical component of various diseases. Historically, patients with hypoalbuminemia of unknown cause were referred to as having idiopathic hypoproteinemia, edema disease, or nephrosis without nephrosis. These patients had neither a decrease in the production of albumin (ie, no signs of malnutrition or hepatic disease) nor an increase in albumin losses from the respiratory tract, kidneys, or skin.
In 1949, Albright et al demonstrated an increase in protein turnover in patients with protein-losing enteropathy. In 1958, Citrin et al were the first to use radiolabeled tracers to demonstrate the actual loss of a protein-containing fluid into the GI tract. Several additional diagnostic techniques using radiolabeled substrates were developed, but a major advance was made when Crossley and Elliot demonstrated that measurement of alpha1-antitrypsin (A1-AT) levels in the stool was a reliable and simple test for protein-losing enteropathy. This approach has identified various conditions that have subclinical protein-losing enteropathy as a component of the disease process.
http://www.jbc.org/content/281/12/7809.full.pdf
Protein Losing Enteropathy Seen in Vitro with Heparan Sulfate
Heparan Sulfate Plays a Central Role in a Dynamic in Vitro
Model of Protein-losing Enteropathy
*
Received for publication, September 30, 2005, and in revised form, December 19, 2005 Published, JBC Papers in Press, January 24, 2006, DOI 10.1074/jbc.M510722200
Lars Bode
Simon Murch
and Hudson H. Freeze
From the
Burnham Institute for Medical Research, Glycobiology and Carbohydrate Chemistry Program, La Jolla, California 92037
and
§
Warwick Medical School, Clinical Sciences Research Institute, Coventry CV2 2DX, United Kingdom
Protein-losing enteropathy (PLE), the loss of plasma proteins
through the intestine, is a symptom in ostensibly unrelated diseases.
Emerging commonalities indicate that genetic insufficiencies predispose for PLE and environmental insults, e.g. viral infections and
inflammation, trigger PLE onset. The specific loss of heparan sulfate (HS) from the basolateral surface of intestinal epithelial cells
only during episodes of PLE suggests a possible mechanistic link.
In
the first tissue culture model of PLE using a monolayer of intestinal
epithelial HT29 cells, we proved that HS loss directly causes protein
leakage and amplifies the effects of the proinflammatory cytokine
tumor necrosis factor (TNF). Here, we extend our in vitro model
to assess the individual and combined effects of HS loss, interferon (IFN), TNF, and increased pressure, and find that HS
plays a central role in the patho-mechanisms underlying PLE.
Increased pressure, mimicking venous hypertension seen in postFontan PLE patients, substantially increased protein leakage, but
HS loss, IFN, or TNF alone had only minor effects. However,
IFN up-regulated TNFR1 expression and amplified TNF-induced protein leakage. IFN and TNF compromised the integrity
of the HT29 monolayer and made it more susceptible to increased
pressure. HS loss itself compromises the integrity of the monolayer,
amplifying the effects of pressure, but also amplifies the effects of
both cytokines.
In the absence of HS a combination of increased
pressure, IFN, and TNF caused maximum protein leakage. Soluble heparin fully compensated for HS loss, providing a reasonable
explanation for patient favorable response to heparin therapy.
http://drugline.org/img/ail/125_126_2.jpg
Protein-losing enteropathy is an abnormal loss of protein from the digestive tract or the inability of the digestive tract to absorb proteins.
Causes
There are many causes of protein-losing enteropathy. Any condition that causes serious inflammation in the intestines can lead to protein loss. Some of the more common causes are:
celiac disease
Crohn's disease
Lymphoma
MUST READ: AUTISM TRIGGER OF GUT DISEASE CAUSED BY SHOTS
REAL MEDICAL JOURNAL!!! GLUTEN INTOLERANCE CAUSED BY HEP B
http://hepatmon.com/?page=article&article_id=387
Bacteria or parasite infection Are Hepatitis B Virus and Celiac Disease Linked?
Salvatore Leonardi
Department of Pediatrics, University of Catania, Catania, Italy
Mario La Rosa
Department of Pediatrics, University of Catania, Catania, Italy
Correspondence:
Salvatore Leonardi MD
Affiliation: Department of Pediatrics, University of Catania
City, Province: Catania,
Country: Italy
Tel: +39 095 378 2764
Fax: +39 095 378 2764
E-mail: leonardi@unict.it
Background and Aims: It has been hypothesized that nonintestinal inflammatory diseases such as hepatitis B virus (HBV) and hepatitis C virus (HCV) may trigger immunologic gluten intolerance in susceptible people. This hypothesis suggests a possible epidemiological link between these two diseases, although this assumption is still a matter of debate.
Methods: We conducted a retrospective study to assess the prevalence of celiac disease in HBV carrier patients who had been infected in childhood.
Results: None of the HBV carrier patients had immunoglobulin A antiendomysium and immunoglobulin A anti-tissue transglutaminase, but 6 patients and 1 recovered subject had immunoglobulin A antigliadin and/or immunoglobulin G antigliadin. Moreover, no patient treated with interferon therapy showed any serological marker of celiac disease.
Conclusions: Due to the small sample size, we cannot claim that there is no association between celiac disease (CD) and HBV, although in our study we did not find any CD patients. A sample size that is more representative of the prevalence of CD in Italy would better support the establishment of any possible connection between CD and HBV.
Keywords: Hepatitis B Virus;Celiac Disease;Enteropathy
__________________________________________________________
If you care about kids and adults who suffer greatly from autism spectrum disorder, please read and try to understand the post above! God Bless you for the great work.
SMART KIDS HAVE SEVERE ALLERGIES
BECAUSE OF THE MAMMALIAN HUMORAL RESPONSE
http://img145.imageshack.us/img145/4296/gifted.png