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"Removing the Doubt is Part of the Cure"
R.E.D. Laboratories was founded in 1998 to develop and commercialize the pioneering work of Dr. Robert Suhadolnik at Temple University who in 1995 discovered the presence of an abnormal protein in a subset of patients with Chronic Fatigue Syndrome (CFS). This protein is related to a normal enzyme, Ribonuclease L (RNase L), one of the interferon-inducible enzymes, which protects the body during a viral infection. An increased amount of this abnormal protein defines a clinical subset of CFS patients.
In June 1998, to secure the scientific foundation of R.E.D. Laboratories, the Company obtained an exclusive license from Temple University on this technology. Subsequently, the Company began to offer assaying patient specimens for the abnormal protein on a fee-for-service basis.
In 2000 the Company started its own research and development activities on chronic immune diseases. Clinical assay development and research programs at R.E.D. Laboratories now focus on inflammatory mechanisms, oxidative stress, intestinal dysfunctions and viral infections, all disorders that contribute to the onset and pathogenesis of diseases such as CFS, multiple sclerosis, or autoimmune diseases.
As a specialty clinical laboratory, R.E.D. Laboratories now offers up to 26 different diagnostic tests to customers all around the world. In parallel, the Company is also actively engaged in therapeutic development programs, with a particular focus on anti-inflammatory, anti-oxidant and anti-viral compounds.
R.E.D. Laboratories facility in Zellik, Belgium:
Intestinal Dysfunction
http://www.redlabs.be/red-labs/our-science/intestinal-dysfunction.php
... Dysbiosis is a frequent disorder of intestinal function, i.e. the overgrowth of pathogenic bacteria in the intestine.The adult human intestinal tract is estimated to contain up to 10exp14 viable microorganisms (10 times more than the number of cells that form the body!). Over 50 different genera of bacteria are represented, accounting for more than 500 different species...Intestinal microflora represents an ecosystem of the highest complexity.
This microflora plays critical roles in the digestion and absorption of nutrients, in the synthesis of vitamins (B and K groups) and fatty acids, in the detoxification of ingested chemicals, but also in the regulation of the immune system.
Alterations in the composition of the gut microflora may have serious consequences for the host health. Factors that can affect the microflora include antibiotic use, stress, and diet.
»Antibiotic use is a common cause of major alterations. Dosage, length of administration, spectrum of activity will determine the impact on the microbial flora.
»Psychological stress can also affect the composition of the flora, including a significant decrease in beneficial bacteria (Lactobacilli and Bifidobacteria) and an increase in pathogenic E. coli. Stress may affect bacterial growth by significantly reducing the mucosal production of mucopolysaccharides and mucins, which are important for inhibiting the adherence of pathogenic organisms, and by decreasing the production of immunoglobulin A (IgA), which play a crucial role in their elimination. Neurochemicals produced upon psychological stress can also directly enhance the growth of pathogenic organisms: norepinephrine stimulates the growth of Y. Enterocolitica, P. Aeruginosa, and gram-negative bacteria such as E. coli.
»Another factor .. is diet.
Some diets promote the growth of beneficial microorganisms, while others promote harmful microfloral activities. For instance, diets rich in sulfur compounds (dairy products, eggs, certain vegetables, dried fruits...) promote the growth of sulfate-reducing bacteria. Globally it appears that populations consuming the typical Western diet have more anaerobic bacteria, less Enterococci, and fewer yeasts than populations consuming a vegetarian or high complex-carbohydrate diet.
The Immunobilan test is one way to assess the overgrowth of detrimental bacteria (see Intestinal Dysfunction Assays section). This assay measures the presence of IgAs (immunoglobulin A) in the blood. IgAs are typically found in secretions of digestive, respiratory and genitourinary systems. However, in the case of bacterial overgrowth in the small intestine they will be produced in large quantities and some will also be found in the bloodstream. Presence of IgAs is therefore an indicator of intestinal dysbiosis; since IgAs are species-specific the assay can even identify which pathogenic bacterias are over-represented. ...
What is CFS (Chronic Fatigue Syndrome)?
http://www.redlabs.be/red-labs/our-science/chronic-fatigue-syndrome.php
Chronic Fatigue Syndrome (CFS) is also known as myalgic encephalomyelitis (ME), post-viral fatigue syndrome, chronic fatigue and immune dysfunction syndrome.
The disease is characterized by a severe, prolonged fatigue lasting for more than six months. Patients complain of extreme exhaustion; they tire easily in the course of normal activities, and may even be unable to perform normal tasks. Fatigue is accompanied by a number of other symptoms: neurocognitive impairments (memory loss, difficulty in concentrating), muscle pain, headaches, unrefreshing sleep, sore throat, persistent low grade fever, enlarged lymph nodes.
CFS shares overlapping symptomology with several diseases.
Before making a diagnosis of CFS, other specific illnesses in which fatigue is the core symptom (such as hypothyroidism, anemia, Lyme disease, lupus, diabetes, cancer…) must be excluded.
Who gets CFS?
CFS affects between 0.1 and 0.4 percent of the population.
Anybody can get CFS, however women are affected more frequently than men by a ratio of 4:1. People exposed to poor working conditions, or stressful work, seem to face a higher risk for CFS; however stress alone does not cause CFS. The most common age of onset is between 20 and 40 years. CFS can also occur in children and adolescents. ...
Viral Infections
http://www.redlabs.be/red-labs/our-science/viral-infections.php
HERPESVIRIDAE
Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Human herpesvirus 6, 7 and 8 (HHV-6, HHV-7, HHV-8) belong to the family of Herpesviridae. With the exception of HHV-8, these DNA viruses are
highly prevalent and infection occurs usually early in life. After a primary infection which is often unnoticed, herpesviruses will stay in their host for life, in a latent state. However, they may eventually reactivate, particularly in immunocompromised or elderly persons.
Beta-herpesviruses (CMV, HHV-6, HHV-7) are lymphotropic and neurotropic viruses that can target the central nervous system (causing encephalitis) and have immunosuppressive effects. Infections with gamma-herpesviruses (EBV, HHV-8) are linked to the development of cancer.
CYTOMEGALOVIRUS
CMV is transmitted through close personal contact (saliva, blood, breast milk, semen…).
20% of children are already infected before puberty; infection is then common during adolescence. Finally 40 to 100% of the general population will show evidence of prior exposure.
Primary CMV infections in newborns can be very serious, leading to sequelae such as mental retardation, visual defects, deafness, or even death. In older children and adults, primary infection is usually asymptomatic. After infection CMV remains latent in the host and can be reactivated when the immune system is severely impaired. Reactivation of the virus can target the central nervous system (acute encephalitis), damage the retina or have dermatologic manifestations (rash, ulcerative lesions). A pathogenic role of CMV in irritable bowel disease is suspected.
EPSTEIN-BARR VIRUS
EBV infects more than 90% of the world’s adult population.
It is transmitted by salivary contact; the virus first replicates in the epithelium of the oropharynx before infecting B lymphocytes where it will persist for life in a latent state. Primary infection typically occurs within the first years of life and is generally asymptomatic. In developed countries however, primary infection is sometimes delayed until late adolescence, and may then result in mononucleosis (kissing disease).
In most individuals persistence of the virus has no consequences; in some people however EBV is associated with the development of cancer. EBV infections were first found to be associated with Burkitt’s lymphoma (a common cancer affecting children in certain regions of Africa) and have been implicated in Hodgkin’s disease, non-Hodgkin’s lymphoma, and nasopharyngeal carcinoma (in specific Asian regions).
In addition to cancer, EBV has been linked to various immune diseases. By infecting T and NK cells, EBV can cause hemophagocytic syndrome (EBV-AHS).
There is evidence that multiple sclerosis may sometimes occur as a consequence of an EBV infection. Serum antibodies to EBV antigens are found in a subset of chronic fatigue syndrome patients.
HUMAN HERPESVIRUS 6
HHV-6 has a very high prevalence (close to 100% of the world’s population has been exposed). It is transmitted mainly by saliva. Transmission occurs usually within the first two years of life; primary infection is often associated with a febrile condition and sometimes with the onset of roseola (exanthem subitum). Two variants of the virus are known, HHV-6A and HHV-6B. HHV-6 is mainly lymphotropic, infecting a broad range of immune cells including T cells, monocytes, NK cells; however the virus can also infect many other tissues such as brain or liver.
Like other herpesviruses HHV-6 will persist in the host after primary infection.
Viral reactivation occurs mainly in the context of immunosuppressive therapy or disease.HHV-6 has immunomodulatory effects, including suppression of T-cell proliferation and alteration of cytokine production. This immunosuppression may favor the development or progression of other viral infections such as CMV or HIV.
Several studies have reported a possible link between HHV-6 and multiple sclerosis (MS). Reactivation of HHV-6 is also suspected to contribute to the pathogenesis of chronic fatigue syndrome (CFS).
HUMAN HERPESVIRUS 7
HHV-7 is closely related to HHV-6.
Primary infection with HHV-7 usually occurs later in childhood than HHV-6 infection; it can also cause exanthem subitum. It has been suggested that HHV-7 infection could reactivate HHV-6 from latency.
HHV-7 may have a narrower tropism than HHV-6.
The virus efficiently infects and replicates in CD4+ cells; it can be found in brain tissue but at a lower frequency than HHV-6.
Rare cases of neurological complications have been reported following primary infections in children; at the moment, no disease has been etiologically linked to HHV-7 reactivation in adults.
HUMAN HERPESVIRUS 8
Unlike other herpesviruses, HHV-8 prevalence is limited and uneven throughout the world.
Up to 40% of sub-Sahara African population is seropositive; in Mediterranean countries prevalence falls to 10-20%, for only 2-5% in the rest of the world. In areas of high prevalence horizontal transmission (through saliva) does occur but otherwise HHV-8 is principally acquired sexually .
Like the other gammaherpesvirus, EBV, HHV-8 infection is associated with cancer.
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