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Post by kammy on Jan 9, 2010 16:09:57 GMT -5
This is for fun, Banny... there's some sort of mysterious 'wood critter' that came up close to the house, this is the patio... wonder what it could be? Look how it starts out on one leg from behind the bush... then see where it steps and how much further apart its stance gets to be?... I've never noticed anything in nature that spreads its legs wider as it walks... have you? ;D  And, the footprints abruptly end... Jeany thinks it's a hopping bird/crow or a rabbit... anyone else? ;D |
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Post by kammy on Jan 9, 2010 16:29:06 GMT -5
Barb sent me a link on an article written by Dr. Sean Abbott on fungi and spores, I can't find it right now... it was basically what we read, text book, about how insects can carry fungal spores and disperse them, etc.
I wrote Barb back and said something like... 'Yada, yada, the same ole, same ole... where does it read about the insects hatching out of the baculovirus that are inside the fungal spores?'
And, I realize that very few really know what I'm trying to say here on this thread and it's my fault, I haven't presented it very well. I thought to myself, why not create a web page trying to describe what I believe I see happening with certain Morgellons experiments and since we're in email contact with Dr. Abbott - send him the link and maybe he will read it?
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Post by kammy on Jan 9, 2010 16:35:06 GMT -5
Oh! The bird flew in on one end... hopped up to the bush, turned around and hopped to the other end of the tracks - then flew away... it's a one legged crow? ;D
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Post by jeany on Jan 11, 2010 19:51:15 GMT -5
Interesting!..
Moth genes are being fused with potatoes?..Arctic Char genes are being fused with strawberries?..what else?..oh..Flounder genes are being fused with tomatoes?..Firefly genes with corn...
BAD SEED: The Dangerous Truth About Our Food
Monsanto is the 'dealer'!
Jeany
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Post by jeany on Jan 12, 2010 13:52:29 GMT -5
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Post by kammy on Jan 12, 2010 15:52:32 GMT -5
The Spheres? Yo Frito! You around? I believe you asked me recently if I was seeing the Neutrophils? Here's a photo of my blood after cutting my finger at 100x on a slide... I think one that the arrow is pointing to is a neutrophil? (Where's all my white blood cells?)  I also think this is similar to the other spheres we're seeing? |
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Post by kammy on Jan 12, 2010 19:40:54 GMT -5
My ear is loaded with granules - I see that the neutrophils not functioning properly can cause granular disease. We know that our lesions aren't having the normal immune response and we can see neutrophils naturally create a fiber network called "NETs"... Neutrophil granulocyte en.wikipedia.org/wiki/Neutrophil_granulocyte"Neutrophils are normally found in the blood stream. However, during the beginning (acute) phase of inflammation, particularly as a result of bacterial infection and some cancers[4][5], neutrophils are one of first-responders of inflammatory cells to migrate toward the site of inflammation, firstly through the blood vessels, then through interstitial tissue, following chemical signals (such as Interleukin-8 (IL-8), Interferon-gamma (IFN-gamma), and C5a) in a process called chemotaxis. The stated normal range for human blood counts varies between laboratories, but a neutrophil count of 2.5-7.5 x 109/L is a standard normal range. Neutrophils are much more numerous than the longer-lived monocyte/macrophage phagocytes. A pathogen (disease-causing microorganism or virus) is likely to first encounter a neutrophil. Some experts hypothesize that the short lifetime of neutrophils is an evolutionary adaptation. The short lifetime of neutrophils minimizes propagation of those pathogens that parasitize phagocytes, the more time such parasites spend outside a host cell, the more likely they will be destroyed by some component of the body's defenses. Also, because neutrophil antimicrobial products can also damage host tissues, their short life limits damage to the host during inflammation. In addition to recruiting and activating other cells of the immune system, neutrophils play a key role in the front-line defence against invading pathogens. Neutrophils have three strategies for directly attacking micro-organisms: phagocytosis (ingestion), release of soluble anti-microbials (including granule proteins) and generation of neutrophil extracellular traps (NETs) [8]." Neutrophil Extracellular Traps - NETs en.wikipedia.org/wiki/Neutrophil_extracellular_traps"Neutrophil extracellular traps (NETs) are networks of extracellular fibres generated by neutrophils that bind pathogens.[1] More recently, it has also been shown that not only bacteria but also pathogenic fungi such as Candida albicans induces neutrophils to form NETs that capture and kill C. albicans hyphal as well as yeast-form cells. NETs may serve as a physical barrier that prevents further spread of the pathogens. While it was originally proposed that NETs would be formed in tissues at a site of bacterial/yeast infection, NETs have also been shown to form within blood vessels during sepsis (specifically in the lung capillaries and liver sinusoids). These observations suggest that NETs might play an important role in the pathogenesis of infectious and inflammatory disorders." |
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Post by kammy on Jan 12, 2010 20:00:29 GMT -5
Chronic granulomatous disease en.wikipedia.org/wiki/Chronic_granulomatous_disease"Chronic granulomatous disease (CGD) (also known as "Bridges–Good syndrome," "Chronic granulomatous disorder," and "Quie syndrome"[1]) is a diverse group of hereditary diseases in which certain cells of the immune system have difficulty forming the reactive oxygen compounds (most importantly, the superoxide radical) used to kill certain ingested pathogens.[2] This leads to the formation of granulomata in many organs.[3] CGD affects about 1 in 200,000 people in the United States, with about 20 new cases diagnosed each year.[4][5] The underlying cellular mechanism that causes chronic granulomatous disease was discovered in 1967, and research since that time has further elucidated the molecular mechanisms underlying the disease.[8] Chronic granulomatous disease is the name for a genetically heterogeneous group of immunodeficiencies. The core defect is a failure of phagocytic cells to kill organisms that they have engulfed because of defects in a system of enzymes that produce free radicals and other toxic small molecules. There are several types, including chronic X-linked disease, chronic b-negative disease, X-linked cytochrome b-positive disease, x-linked variant disease, and atypical granulomatous disease[9]. Symptoms Classically, patients with chronic granulomatous disease will suffer from recurrent bouts of infection due to the decreased capacity of their immune system to fight off disease-causing organisms. The recurrent infections they acquire are specific and are, in decreasing order of frequency: * pneumonia * abscesses of the skin, tissues, and organs * suppurative arthritis * osteomyelitis * bacteremia/fungemia * superficial skin infections such as cellulitis or impetigo Most people with CGD are diagnosed in childhood, usually before age 5.[10] Early diagnosis is important since these people can be placed on antibiotics to ward off infections before they occur. Atypical infectionsPeople with CGD are sometimes infected with organisms that usually do not cause disease in people with normal immune systems. Among the most common organisms that cause disease in CGD patients are: * bacteria (particularly those that are catalase-positive)[11] o Staphylococcus aureus. o Serratia marcescens. o Salmonella species. o Klebsiella species. o Pseudomonas cepacia, a.k.a. Burkholderia cepacia.[12] o Nocardia.[13] * fungi o Aspergillus species. Aspergillus has a propensity to cause infection in people with CGD and of the Aspergillus species, Aspergillus fumigatus seems to be most common in CGD. o Candida species.  Microscopic image of the fungus, Aspergillus fumigatus, an organism that commonly causes disease in people with chronic granulomatous disease. [10] The affected gene on the X chromosome codes for the gp91 protein p91-PHOX (p is the weight of the protein in kDa; the g means glycoprotein). CGD can also be transmitted in an autosomal recessive fashion (via CYBA and NCF1) (*??) and affects other PHOX proteins. The type of mutation that causes both types of CGD are varied and may be deletions, frame-shift, nonsense, and missense.(*??)[14][15] A low level of NADPH, the cofactor required for superoxide synthesis, can lead to CGD. This has been reported in women who are homozygous for the genetic defect causing glucose-6-phosphate dehydrogenase deficiency (G6PD), which is characterised by reduced NADPH levels. Pathophysiology Phagocytes (i.e., neutrophils, monocytes, and macrophages) require an enzyme to produce reactive oxygen species to destroy bacteria after they ingest the bacteria in a process called phagocytosis, a process known as the respiratory burst. This enzyme is termed "phagocyte NADPH oxidase" (PHOX). The initial step in this process involves the one-electron reduction of molecular oxygen to produce superoxide anion, a free radical. Superoxide then undergoes a further series of reactions to produce products such as hydrogen peroxide, hydroxyl radical and hypochlorite (bleach). The reactive oxygen species this enzyme produces are toxic to bacteria and help the phagocyte kill them once they are ingested. In particular, individuals are vulnerable to infections with catalase positive organisms. Defects in one of the four essential subunits of this enzyme can all cause CGD of varying severity, dependent on the defect. There are over 410 known possible defects in the PHOX enzyme complex that can lead to chronic granulomatous disease[3]. DiagnosisThe nitroblue-tetrazolium (NBT) test is the original and most widely-known test for chronic granulomatous disease.[16] It is negative in CGD, and positive in normal individuals. This test depends upon the direct reduction of NBT by superoxide free radical to form an insoluble formazan. This test is simple to perform and gives rapid results, but only tells whether or not there is a problem with the PHOX enzymes, not how much they are affected. A similar test uses dihydrorhodamine (DHR); whole blood is stained with DHR, incubated, and stimulated produce superoxide radicals which reduce DHR to rhodamin in cells with normal function. An advanced test called the cytochrome C reduction assay tells physicians how much superoxide a patient's phagocytes can produce. Once the diagnosis of CGD is established, a genetic analysis may be used to determine exactly which mutation is the underlying cause. Antibiotics Physicians often prescribe the antibiotic trimethoprim-sulfamethoxazole to prevent bacterial infections.[17] This drug also has the benefit of sparing the normal bacteria of the digestive tract. Fungal infection is commonly prevented with itraconazole,[18] although a newer drug of the same type called voriconazole may be more effective.[19] The use of this drug for this purpose is still under scientific investigation. Immunomodulation Interferon, in the form of interferon gamma-1b (Actimmune) is approved by the Food and Drug Administration for the prevention of infection in CGD. It has been shown to prevent infections in CGD patients by 70% and to reduce their severity. Although its exact mechanism is still not entirely understood, it has the ability to give CGD patients more immune function and therefore, greater ability to fight off infections. This therapy has been standard treatment for CGD for several years.[20] Hematopoietic stem cell transplantation (HSCT) Hematopoietic stem cell transplantation from a matched donor is potentially curative. The procedure is controversial, and not without significant risk [21] Prognosis There are currently no studies detailing the long term outcome of chronic granulomatous disease with modern treatment. Without treatment children often die in the first decade of life. Available data indicates that X linked CGD is more severe, with most treated patients dying in the third or fourth decade of life [22]. Epidemiology CGD affects about 1 in 200,000 people in the United States, with about 20 new cases diagnosed each year.[4][5] Chronic granulomatous disease affects all people of all races, however, little information on prevalence outside of the United States is available. One survey in Sweden reported an incidence of 1 in 220,000 people [22]. Research Gene therapy is currently being studied as a possible treatment for chronic granulomatous disease. CGD is well-suited for gene therapy since it is caused by a mutation in single gene which only affects one body system (the hematopoietic system). Viruses have been used to deliver a normal gp91 gene to rats with a mutation in this gene, and subsequently the phagocytes in these rats were able to produce oxygen radicals.[24] In 2006, two human patients with X-linked chronic granulomatous disease underwent gene therapy and blood cell precursor stem cell transplantation to their bone marrow. Both patients recovered from their CGD, clearing pre-existing infections and demonstrating increased oxidase activity in their neutrophils. However, long-term complications and efficacy of this therapy are unknown.[25]" |
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Post by zabrubon on Jan 12, 2010 20:49:43 GMT -5
Kammy, really good article. However, I was never sick as a child, in fact I was incredibly healthy until about ten years ago. I started to get ill when I was late forty. How can I have this granual disease if it starts when your young?
Or was there something else in this article that I missed?
ChicagoBonnie
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Post by kammy on Jan 12, 2010 20:51:06 GMT -5
I think it would be wise to ask for this nitroblue-tetrazolium (NBT) test or have your doctor for testing for this genetic disorder especially if you are producing 'granules' or 'specks'. And, if positive, follow up with the the cytochrome C reduction assay test. And, especially if you've had any reports of granular, benign cancer, atypical cells or pseudo-cancer in your biopsies. I found this statement interesting; "MOST people with CGD are diagnosed in childhood, usually before age 5." If Morgellons is a type of chronic granulomatous disease, why are we just now showing it in our 30's, 40's, 50's...? It's says "most"... ? Possibly, we have this "X-linked trait" genetic factor and our health has been good enough to ward the disease off until... ? We know Morgellons is more than one known disease - what about the insects, the baculovirus... well - do a patent search on "neutrophil baculovirus"... there's 9,863 patents - (it needs to be narrowed down.) tinyurl.com/yzb489j |
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Post by kammy on Jan 12, 2010 21:14:14 GMT -5
Kammy, really good article. However, I was never sick as a child, in fact I was incredibly healthy until about ten years ago. I was seldom sick as a child. I started to get ill when I was late forty. Or was there something else in this article that I missed? ChicagoBonnie Hi Bonnie - I was posting the above answer while you were posting... Hello! Also, we've finding that some of us are being told that we have cancer, "atypical cells', a granular form of cancer or adenocarcinoma... what we're thinking is really pseudo-adenocarcinoma, that's not really cancer but is 'cancer-like'. (Barb is noting how a particular parasite can give pseudo-adenocarcinoma results, also.) Frito, Barb and Jeany need to look at this info above and give their opinions, IMO, they are much more knowledgeable about what is happening within the human body against what we're seeing and learning from others. We've had a good health system and food in the U.S. in our childhoods and young adulthood, it's only recently that 'things' have gotten out of hand with food modifications, in particular. Is something they have introduced that has caused our hidden genetic defect to 'kick in' with us that are susceptible to this granular-type disease? First, we have to figure out what Morgellons is, unfortunately we're having to lead our doctors, they appear 'lost', and when we start getting confirmation through testing - then... we can better pinpoint what caused Morgellons to happen. I think CGD is a good place to look to either confirm or rule out? |
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Post by kammy on Jan 12, 2010 21:34:01 GMT -5
Let's look at the Case Study Definition on the morgellons.org site again to see how this above information might pertain to us: morgellons.org/case_definition.htm"Common Laboratory Abnormalities Elevated cytokines: TNF-alpha, IL-6, TGF-beta; Elevated inflammation markers: C-reactive protein and TNF-alpha; Immunodeficiency markers: low CD 56 or CD 57 number, low C1Q, low IgG subclasses 1 and 3; Hematological abnormalities: low hemoglobin and hematocrit with abnormal RBC indices; and Biochemical abnormalities: elevated blood glucose, insulin, calcium, and serum Homocysteine, and low serum potassium and magnesium. The consistent finding of numerous unexpected biologic agents at atypically high levels (some thought to be non-pathogens, others definitely pathogenic) strongly supports that an immune deficiency state exists in Morgellons patients. Agents identified serologically include many zoonoses (intermittently and in low numbers) such as Borrelia (at least five species) and Babesia, a single recently found gram negative bacterium, most herpes viruses, some strongly activated such as VZV and HHV-6, several mycology species (esp. Tineas), and particularly in those we have labeled Morgellons patients, parasites (species will be elaborated following PCR sequencing)." |
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Post by kammy on Jan 12, 2010 22:26:41 GMT -5
Chronic granulomatous disease (CGD) and Morgellons
- A Comparison From M.org - "strongly supports that an immune deficiency state exists in Morgellons patients." "CGD is well-suited for gene therapy since it is caused by a mutation in single gene which only affects one body system (the hematopoietic system)." Haematopoiesis en.wikipedia.org/wiki/Hematopoietic_system"Haematopoiesis sometimes also haemopoiesis or hemopoiesis is the formation of blood cellular components. All cellular blood components are derived from haematopoietic stem cells. The ability of the bone marrow to regulate the quantity of different cell types to be produced is more accurately explained by a stochastic theory: Undifferentiated blood cells are determined to specific cell types by randomness. The hematopoietic microenvironment prevails upon some of the cells to survive and some, on the other hand, to perform apoptosis and die. By regulating this balance between different cell types, the bone marrow can alter the quantity of different cells to ultimately be produced. Haematopoietic growth factors Red and white blood cell production is regulated with great precision in healthy humans, and the production of granulocytes is rapidly increased during infection. Chronic granulomatous disease is the name for a genetically heterogeneous group of immunodeficiencies." ----------------------------------- From M.org - "Elevated cytokines: TNF-alpha, IL-6, TGF-beta;" One reason for elevated cytokines is inflammation: en.wikipedia.org/wiki/Inflammation Neutrophils migrate from blood vessels to the inflamed tissue via chemotaxis, where they remove pathogens through phagocytosis and degranulationCytokines from injured cells induce the expression of E-selectin on endothelial cells, which functions similarly to P-selectin. Cytokines also induce the expression of integrin ligands on endothelial cells, which further slow leukocytes down. These weakly bound leukocytes are free to detach if not activated by chemokines produced in injured tissue. Activation increases the affinity of bound integrin receptors for ligands on the endothelial cell surface, firmly binding the leukocytes to the endothelium. Immune reactions due to hypersensitivity----------------------------------- From M.org - "The consistent finding of numerous unexpected biologic agents at atypically high levels (some thought to be non-pathogens," "People with CGD are sometimes infected with organisms that usually do not cause disease in people with normal immune systems." ----------------------------------- From M.org - "several mycology species (esp. Tineas)" "Among the most common organisms that cause disease in CGD patients are: o Aspergillus species. Aspergillus has a propensity to cause infection in people with CGD and of the Aspergillus species, Aspergillus fumigatus seems to be most common in CGD. o Candida species." ----------------------------------- From M.org - "1. “Filaments” are reported in and on skin lesions and at times extruding from intact-appearing skin." "Neutrophil extracellular traps (NETs) are networks of extracellular fibers generated by neutrophils that bind pathogens."  Stock photo of macrophage (NETs) at Imageshack: ----------------------------------- They seem to have a lot in common? Note that "immune reactions to hypersensitivity" is mentioned under inflammation. Jeany has a theory about Morgellons and hypersensitivity she has been researching and will present soon. |
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Post by kammy on Jan 12, 2010 23:02:03 GMT -5
Remember the other day I said I had an ulcer on my tongue? Here is a stock photo... this IS NOT my tongue, mine didn't look this bad:  Cyclic neutropenia. neutropenia a diminished number of neutrophils in the blood. Where are our white blood cell counts? Also, is your LDL (good) cholesterol on the low side? |
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Post by kammy on Jan 12, 2010 23:36:47 GMT -5
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Post by kammy on Jan 12, 2010 23:54:04 GMT -5
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Post by skytroll on Jan 13, 2010 0:40:38 GMT -5
E- selectin
P- selectin
from the link above, Kammy it appears these two selectins have some
significance to the activiation of cytokines.
from you link: ....." Cytokines from injured cells induce the expression of E-selectin on endothelial cells, which functions similarly to P-selectin. Cytokines also induce the expression of integrin ligands on endothelial cells,"..............======================= so E-selectin expression
integrin ligand expression from cytokines.==================================== E-selectin, also known as CD62E, is a cell adhesion molecule expressed only on endothelial cells activated by cytokines. Like other selectins, it plays an important part in inflammation. In humans, E-selectin is encoded by the SELE gene.Ligands E-selectin recognizes and binds to sialylated carbohydrates present on the surface proteins of certain leukocytes. These carbohydrates include members of the Lewis X and Lewis A families found on monocytes, granulocytes, and T-lymphocytes
FunctionDuring inflammation, E-selectin plays an important part in recruiting leukocytes to the site of injury. The local release of cytokines IL-1 and TNF by damaged cells induces the over-expression of E-selectin on endothelial cells of nearby blood vessels.[2] Leukocytes in the blood expressing the correct ligand will bind with low affinity to E-selectin, causing the leukocytes to "roll" along the internal surface of the blood vessel as temporary interactions are made and broken. As the inflammatory response progresses, chemokines released by injured tissue enter the blood vessels and activate the rolling leukocytes, which are now able to tightly bind to the endothelial surface and begin making their way into the tissue.[2]
P-selectin has a similar function, but is expressed on the endothelial cell surface within minutes as it is stored within the cell rather than produced on demand.[2] [edit] Pathological relevance In cases of elevated blood glucose levels, such as in sepsis, E-selectin expression is higher than normal, resulting in greater microvascular permeability. The greater permeability leads to edema of the skeletal endothelium, resulting in skeletal muscle ischemia and eventually necrosis. This underlying pathology is the cause of the symptomatic disease critical illness polyneuromyopathy (CIPNM).[3] Traditional Chinese herbal medicines, like berberine downregulate E-selectin.[4] en.wikipedia.org/wiki/E-selectin===================== It seems these are adhesion molecules........that increase whenever inflammation is present form the cytokines. E-selectin and integrin ligand: taking me to Kunjin virus alpha viruses and baculoviruses. This might help Kammy! seems the ti epigenome is what we need to see and what was used. some have more than one thing going on. Note who is involved here: BAXTER evidently looking for a vaccine for ebola and used the ebola kunjin disease in the vaccine. Is in the h1n1 vaccine. Hope this shows how the alpha and baculo are used. I think we can decipher from these reports or abstracts what was in their minds. The Epigenome is big. and so much involved I can tackle the ti epigenome, it began in the plasmid. It is a process and it began way back. Delivery system through the environment, You change the environment, you have changed the people. T1, T2, T3 etc....................... skytroll
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Post by skytroll on Jan 13, 2010 1:51:42 GMT -5
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Post by skytroll on Jan 13, 2010 3:08:06 GMT -5
T1 Novel alphavirus vectors for gene delivery and transgene expression Kenneth Lundstrom F. Hoffmann-La Roche, Research Laboratories, Basel Switzerland Expression vectors based on the replicons of Semliki Forest virus (SFV) and Sindbis virus, two common alphaviruses, have been engineered for efficient gene expression both in vitro and in vivo. Attractive features of alphavirus vectors are the rapid generation of high-titer recombinant virus particles, the broad host range, cytoplasmic RNA replication and extreme levels of recombinant protein expression. Although efficient infection and recombinant protein expression has been established, the high cytotoxicity of alphavirus vectors has restricted their use. Novel less cytotoxic vectors based on site-directed mutagenesis of the SFV nonstructural genes have therefore been engineered. ============================ recombinant virus Particles, that is all that is needed for the vectors. these particles are tracked by: electrophysiological recordings. ================ Earlier studies have demonstrated that SFV-based expression of recombinant G protein-coupled receptors and ligand-gated ion channels produces high specific binding activity and functional responses measured by coupling to G proteins (intracellular Ca2+-release, inositol phosphate accumulation, cAMP stimulation and GTPg S binding) and by electrophysiological recordings. from the list: www.boku.ac.at/IAM/5gdcpe/abstract_book.htmskytroll |
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Post by kammy on Jan 13, 2010 8:19:43 GMT -5
TY, TY! Skytroll!! WTG! I don't have any idea of what you just said... lol - I'm going to have to study... it's seems like we're getting closer... (Frito...Jeany? HELP!) and Skytroll please continue with any input you feel is appropriate, once again, ty!
I'm now thinking that the baculovirus is a middle player in the 'play' we're seeing... the big picture is identifying what's happening on the main stage - and then, I can easily show a doctor, scientist, or you how I believe the baculovirus is operating inside Morgellons, to point the scientists in the right direction and allow them figure it out for sure with scientific testing.
I'm asking for help, especially those that have a medical background and even if you don't - like myself, we can learn. I'm asking the better minds to come together here to help figure this out, I want to be able to give our doctors a good idea of where to look based on what we're seeing and from the data that's out there.
We're all about to see our doctors in the near future - wouldn't it be idea if several of us got tested for a particular genetic defect/syndrome/disorder and we ALL have this in common? That's what makes a disease a disease... what we have in common. Morgellons is complicated in that it appears random and invisible, we know we have common denominators, what are they? Until we can figure it out - we will remain lost.
One 'piece' of knowledge will lead to another and eventually everything will fall into place. The thing is... each one of us has a 'piece' - it's going to take all of us as a team.
(*I'm wondering...why is Morgellons 'invisible'?)
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