Human Anatomy, Physiology, and Medicine. Anything human!
what do we have here ?
http://www.mpg.de/english/illustrations ... index.html
It doesn’t look appetizing: when Ustilago maydis attacks a maize plant, its cobs bear hideous tumours rather than crunchy niblets. So far, no effective means of combating the maize smut pathogen has been found. However, an international team has now made significant progress in the search for a solution. Led by researchers from the Max Planck Institute for Terrestrial Microbiology in Marburg, the scientists have analysed the U. maydis genome. Among the 7,000 genes of the fungus, they have found some with which the fungus lives at the expense of its host plant - without killing it. These genes probably also help the fungus to circumvent the plant’s defences. Researchers are now hoping to apply these findings to other fungi, which like Ustilago maydis depend on living plants (Nature, November 2, 2006).
The Marburg scientists focused on genes which might play a part in infecting the plant and found them in the clusters of secreted proteins. The activity of the genes increases as soon as the fungus infects a plant. "This indicates that the secreted proteins could be effectors, which control the interaction of the fungus with the plant," says Regine Kahmann, Director at the Max Planck Institute in Marburg. In order to confirm this suspicion, her working group performed various experiments, in each case removing one of these twelve clusters from the genome. This revealed that four of the clusters are essential in order for the fungus to develop its full damaging effect. One of the gene clusters, however, clearly helps Ustilago to curb its own aggressiveness: the fungus caused even greater damage to its host when the scientists switched off this ensemble of genes. Refraining from causing too much damage to its host also makes sense for the fungus, because Ustilago maydis relies on the living plant in order to propagate. The fact that Ustilago maydis spares its host as much as possible is also indicated by the number of fungal enzymes that can destroy the cell wall of the plant: Ustilago has just 33; fungi which simply eat their hosts have well over 100.
Ustilago maydis certainly does not present a serious problem to maize farmers, but in recent years it has become a model for other biotrophic fungi, many of which are related to Ustilago maydis. This group of fungi, which also includes rust fungus, causes a lot of trouble for farmers worldwide. However, biologists cannot specifically alter the genes of most of these fungi in the laboratory. "Hopefully our findings on Ustilago maydis can be transferred to this group of fungi," says Kämper.
The mammalian cell constantly receives signals from its surroundings to which it has to respond appropriately. Growth factors, for example, can lead to growth of a cell, its differentiation or proliferation. Defects in these tightly regulated and controlled processes can cause cancer and other human diseases. In recent decades, knowledge of the important players in signal transduction has been painstakingly accumulated, mainly through the study of individual molecules in specific pathways. This approach may fall short though, because the cellular answer to environmental stimuli often doesn’t show on the level of production but the modification of proteins after their synthesis. "Phosphorylation is the most important and most thoroughly researched modification," says Mann. "An estimated one-third of all cellular proteins are affected. Therefore, the dynamic phosphoproteome provides a missing link in a global, integrative view of cellular regulation."
Mann and his team improved and extended a previously developed technology, which enabled them to identify for the first time all phosphorylations of all proteins in living cells - and in their temporal dynamic. For this approach cell cultures were stimulated by EGF for different lengths of time. The "Epidermal Growth Factor" is known for causing the phosphorylation of a multitude of enzymes and proteins along a signal transduction pathway. In the following step all proteins were isolated from the cells, divided into different fractions and analysed via mass spectrometry. This technology allows the precise identification of structure and composition of unknown compounds, here the cellular proteins. In total, 6,600 specific phosphorylation sites in 2,244 proteins were detected. "Comparing our results with the listings in existing databases showed that more than 90 percent of our sites were novel. This suggests that the majority of cellular phosphorylation sites still await identification."
Equally surprising was the discovery that about half of all cellular proteins harbour more than one phosphorylation sites, which in many cases behave differently. "This makes more than one way of phosphorylation possible where proteins serve as integrating platforms for a variety of incoming stimuli", says Mann. "This integration of signals could be independent, with phosphorylation of each site occurring separately from the others. It could also be dependent so that a ‘priming site’ has to be phosphorylated first for the subsequent modification of all other sites in the protein. In any case, the degree of phosphorylation should always be measured site specifically rather than for the protein as a whole". For the efficient use of their results the research team created the Phosida database , where all the phosphorylation sites are listed with additional information and connections to respective listings in other databases. An interesting service for scientists with widely varying expertise, not the least for tumour researchers because they have to investigate defects in cellular signaling which often occurs in progressed forms of cancer. The new technology will allow the search for new data - which might not be necessary too soon. "Our study revealed more phosphorylation sites than all previous studies combined,"
Identification of mycoplasma membrane proteins by
systematic TnphoA mutagenesis of a recombinant library
Catherine M. Cleavinger, Mary F. Kim, Jeong H. Im and Kim S. Wise*
Wall-less prokaryotes in the genus Mycoplasma include over 90 species of infectious agents whose pathogenicity for humans and other animals is currently being assessed. Molecular characterization of surface proteins is critical in this regard but is hampered by the lack of genetic systems in these organisms. We used TnphoA transposition to systematically mutagenize, in Escherichia coli, a genomic plasmid library constructed from Mycoplasma fermentans, a potential human pathogen. The strategy circumvented problems of expressing mycoplasma genes containing UGA (Trp) codons and relied on the construction of the vector pG7ZCW, designed to reduce TnphoA transposition into vector sequences. Functional phoA gene fusions directly identified genes encoding 19 putative membrane-associated proteins of M. fermentans. Sequences of fusion constructs defined three types of export sequence: (1) non-cleavable, membrane-spanning sequences, (2) signal peptides with signal peptidase (SPase) I-like cleavage sites, and (3) signal peptides with SPase II-like lipoprotein-cleavage sites which, like most other mycoplasmal lipoprotein signals analysed to date, differed from those in several Gram-negative and Gram-positive eubacteria in their lack of a Leu residue at the 3 position. Antibodies to synthetic peptides that were deduced from two fusions to predicted lipoproteins, identified corresponding amphiphilic membrane proteins of 57 kDa and 78 kDa expressed in the mycoplasma. The P57 sequence contained a proline-rich N-terminal region analogous to an adhesin of Mycoplasma gallisepticum. The P78 protein was identical to a serologically defined phase-variant surface lipoprotein. TnphoA mutagenesis provides an efficient means of systematically characterizing functionally diverse lipoproteins and other exported proteins in mycoplasmas.
Full PDF paper:
This paper was presented at a colloquium entitled “Genetics and the Origin of Species” organized by Francisco J.Ayala (Co-chair) and Walter M.Fitch (Co-chair), held January 30 to February 1, 1997, at the National Academy of Sciences Beckman Center in Irvine, CA.
Transposable elements as sources of variation in animals and plants
MARGARET G.KIDWELL* AND DAMON LISCH
Department of Ecology and Evolutionary Biology and The Center for Insect Science. University of Arizona, Tucson, AZ 85721
ABSTRACT A tremendous wealth of data is accumulating on the variety and distribution of transposable elements (TEs) in natural populations. There is little doubt that TEs provide new genetic variation on a scale, and with a degree of sophistication, previously unimagined. There are many examples of mutations and other types of genetic variation associated with the activity of mobile elements. Mutant phenotypes range from subtle changes in tissue specificity to dramatic alterations in the development and organization of tissues and organs. Such changes can occur because of insertions in coding regions, but the more sophisticated TE-mediated changes are more often the result of insertions into 5' flanking regions and introns. Here, TE-induced variation is viewed from three evolutionary perspectives that are not mutually exclusive. First, variation resulting from the intrinsic parasitic nature of TE activity is examined. Second, we describe possible coadaptations between elements and their hosts that appear to have evolved because of selection to reduce the deleterious effects of new insertions on host fitness. Finally, some possible cases are explored in which the capacity of TEs to generate variation has been exploited by their hosts. The number of well documented cases in which element sequences appear to confer useful traits on the host, although small, is growing rapidly.
The book whose publication we are celebrating in this colloquium indicates that Theodosius Dobzhansky had a very special interest in gene mutation and its causes. Dobzhansky recognized mutation as the “raw material” on which natural selection acts and as the first of three steps necessary for evolution to take place. However, the discovery of transposable elements (TEs) in the 1940s by Barbara McClintock occurred a decade later, and it was a further 30 years before the significance of her findings started to be fully appreciated. Sixty years ago, Dobzhansky was well aware of the mutagenic properties of ionizing radiation discovered in 1927 by H.J.Muller but acknowledged that much less than 1% of spontaneous mutations were attributable to this cause. He distinguished between spontaneous and induced mutations: “The former are those which arise in strains not consciously exposed to known or suspected mutation-producing agents.” He also pointed out that “since the name spontaneous constitutes only a thinly-veiled [sic] admission of the ignorance of the phenomenon to which it is applied, the quest for the causes of mutation has always occupied the attention of geneticists.” Although at that time no clues to its nature were yet available, Dobzhansky realized that a major piece of the mutation puzzle was still missing. We believe he would have been intrigued with the discoveries of TEs in natural populations that have taken place during the last 20 years and that he would have been an active participant in the continuing debate about their role in evolution.
Distribution and Classification
TEs are discrete segments of DNA that are distinguished by their ability to move and replicate within genomes. Since their discovery by Barbara McClintock ˜50 years ago (1), TEs have been found to be ubiquitous in most living organisms. They comprise a major component of the middle repetitive DNA of genomes of animals and plants. They are present in copy numbers ranging from just a few elements to tens, or hundreds, of thousands per genome. In the latter case, they can represent a major fraction of the genome, especially in some plants. For example, TEs recently have been estimated to make up >50% of the maize genome (2). In Drosophila, ˜10–15% of the genome is estimated to be made up of TEs, most of which are found in distinct regions of centric heterochromatin (3).
TEs are classified in families according to their sequence similarity. Two major classes are distinguished by their differing modes of transposition (4). Class I elements are retroelements that use reverse transcriptase to transpose by means of an RNA intermediate. They include long terminal repeat retrotransposons and long and short interspersed elements (LINES and SINES, respectively). Long terminal repeat retrotransposons are closely related to other retroelements of major interest, such as retroviruses (5). The gypsy element in Drosophila is an example of a rare type of retrotransposon that can sometimes also behave as a retrovirus (6).
Class II elements transpose directly from DNA to DNA and include transposons such as the Activator-Dissociation (Ac-Ds) family in maize, the Tam element in Antirrhinum, the P element in Drosophila, and the Tc1 element in the worm, Caenhorabditis elegans. Recently, a category of TEs has been discovered (7) whose transposition mechanism is not yet known. These miniature inverted-repeat TE (MITEs) have some properties of both class I and II elements. They are short (100–400 bp in length), and none so far has been found to have any coding potential. They are present in high copy number (3,000–10,000) per genome and have target site preference for TAA or TA in plants. MITEs such as the Tourist element in maize and the Stowaway element in Sorghum (7) are found frequently in the 5' and 3' noncoding regions of genes and are frequently associated with the regulatory regions of genes of diverse flowering plants. TEs with similar properties also have been described in Xenopus (8), humans (9, 10), and the yellow fever mosquito, Aedes aegypti (11). Most, but not all, TE families are made up of both autonomous and nonautonomous elements.
Seems more complicated it is, the more the natural body, loses its hold.
Gene altering and physics. What a combination. Electrical pulses, magnetic movements, Wow. We are one with the Earth.
Seem to like the fat cells.
The fibers can easily go through the fat, if heated.
Is this a way to lose weight? Ha ha.
"Excerpt from article found here:"
Gene disruption mediated by transposable elements or transposons that occur in a variety of organisms including zebrafish may be another useful approach for the identification of novel mutant phenotypes and the rapid assignment of gene function. Evidence for the application of this approach to identify pigment-related genes in fish has been provided by a number of reports investigating albino mutants in medaka. In these studies, the three mutant alleles (i1, i4, and ib) responsible for an albino phenotype are all a result of mutations that occurred by the insertion of the transposable elements Tol1 (i1) or Tol2 (i4 and ib) into the tyrosinase gene (i locus) (42, 88, 89). Despite a current lack of understanding regarding the multiple insertions of these members of the hobo/Ac/Tam (hAT) transposon family into the tyrosinase gene, the i locus mutants of medaka provide an interesting model for the study of melanin synthesis in fish. Demonstration of germline transmission using transposons such as Tol2 (45) and Sleeping Beauty (SB) (90), a member of the Tc1/mariner family, highlights the potential of transposons for zebrafish transgenesis, mutagenesis, and application to functional genomics.
Tc1/mariner transposons, such as SB, are suited for insertional mutagenesis as a result of minimal requirements for host cell factors and characteristics of integration target sites. These transposons self-excise and reintegrate elsewhere using a cut and paste mechanism facilitated by an element- or exogenous-encoded transposase (91). The (re)mobilization of a transposon to a new location generates simple, reproducible lesions. Integration loci are easily detected (92) and are not confounded by multicopy concatemers or other complex rearrangements associated with plasmid-based transgenesis. As a result, marking genes by transposon integration facilitates cloning and further molecular characterization of that gene (90). With appropriate modification, transposons, such as SB or Tol2, may be used for gene trapping and insertional mutagenesis of zebrafish (90, 93). Enhancer traps, gene traps, and other traps based on these systems have significant promise for gene discovery in a variety of biological processes including pigmentation.
The completion of the human genome has ushered in a new era focused on understanding the relationship between gene function and human disease. Functional genomics is increasingly seen as a way toward understanding genes in isolation and within the complex networks in which genes interact. High-throughput technology for expression analysis (e.g. microarrays or proteomic approaches) facilitates identification of gene sets enriched for candidates with high relevance to a particular biological or disease process. Through the trans-NIH initiatives and multi-species genome sequencing efforts, a variety of animal models including zebrafish (14) are providing the basis for functional genomics through comparative analysis between model genetic organisms and humans. With an array of pigmentation mutants from large-scale mutagenesis screens and ever increasing methods for genetic analysis and transgenesis, the zebrafish is well-suited to this new paradigm and will continue to be an invaluable model to improve the understanding of pigment cell biology and disease.
29. Kelsh RN, Brand M, Jiang YJ, Heisenberg CP, Lin S, Haffter P, Odenthal J, Mullins MC, van Eeden FJ, Furutani-Seiki M, Granato M, Hammerschmidt M, Kane DA, Warga RM, Beuchle D, Vogelsang L, Nusslein-Volhard C. Zebrafish pigmentation mutations and the processes of neural crest development. Development 1996;123: 369–389
34. Haffter P, Odenthal J, Mullins MC, Lin S, Farrel MJ, Vogelsang E, Hass F, Brand M, van Eeden FJ, Furutani-Seiki M, Granato M, Hammerschmidt M, Heisenberg CP, Jiang YJ, Kane DA, Kelsh RN, Hopkins N, Nusslein-Volhard C. Mutations affecting pigmentation and shape of adult zebrafish. Dev Genes Evol 1996;206: 260–276
38. Haffter P, Granato M, Brand M, Mullins MC, Hammerschmidt M, Kane DA, Odenthal J, van Eeden FJ, Jiang YJ, Heisenberg CP, Kelsh RN, Furutani-Seiki M, Vogelsang E, Beuchle D, Schach U, Fabian C, Nusslein-Volhard C. The identification of genes with unique and essential functions in the development of the zebrafish, Danio rerio. Development 1996;123: 1–36
I am truly sorry that some people feel that
no one is reading their posts. I know I
read every one of them with Randy’s being
the only exception (I’m tired of being screamed
at and talked down to .) Can’t say that I
read every single day or that I hit every link,
but I try. Some posts I do not relate to and
some I do. Sometimes I do have a comment
but still, for one reason or another, do not post it.
I cannot post about every new post but if you
want an opinion from me then please address
me personally and I will make every effort to
respond. Remember, I am reading so I will
see that I am being addressed. I am not the
smartest or the brightest here but I am honest
and sincere and will do my best to help anyone
of you. Again, I am sorry that you guys feel that
way, it is certainly not true, and I hope this can
resolve some of this issue for you all. Each one
of you, with only one exception as stated above,
are valued here whether you realize it or not.
Just wanted to let you know that your spreadsheet,
data collecting is a wonderful idea, sorry I did not
post that earlier. I would like to work on this with you.
Thanks for the update on Reliefseeker. Hope she is well.
WOW , I did not know about the tam element!
So, what do you get if you times tam by 2.. ...??????
“Molecular analysis of paramutant plants of Antirrhinum
majus and the involvement of transposable elements
Summary Paramutation is observed when the Antirrhinum majus lines 44 and 53 are crossed. These two lines both have insertions at the nivea locus, which encodes chalcone synthase (chs). The allele niv-53 carries the transposable element Tam1 in the promoter region of the chs gene; niv-44 carries the element Tam2 within the gene. The Tam1 element has previously been extensively characterised. Here the Tam2 element is further characterised, and the arrangement of the nivea locus in paramutant plants is analysed. The complete sequence of Tam2, and that of a partial cDNA complementary to it, have been determined. The cDNA is probably transcribed from a different copy of Tam2 from that present at the nivea locus, and does not encode a functional protein. Genomic Southerns of F1 plants from the 53/44 cross show that no major rearrangements are consistently associated with paramutation at the nivea locus of A. majus. The isolation from a paramutant plant arising from a 53/44 cross of an allele (niv-4432) resulting from the excision of Tam2 is reported. The excision of Tam2 resulted in a 32 bp deletion of chs gene sequences. Plants homozygous for the new niv-4432 allele have white flowers and are still paramutagenic, demonstrating that Tam2 need not be present at the nivea locus for paramutation to occur. Different interactions between Tam1 and Tam2 are discussed, and a possible model for paramutation is presented.
Key words Tam1 - Tam2 - Paramutation - DNA rearrangement"
Glad to see you post and I hope you have
that server problem figured out.
You can still listen to the Rense programs if you
missed one of them. The last one has Dr. Staniger
talking about how this might take DNA from our
environment and use it to replicate its self. I have
heard many people infected suspect this same thing,
it is very interesting so be sure to listen.
Tams father is a scientist and Tam is a poet.
Funny Sabrina that you will read endless garbage with no real anything in site expcept the sounds of the posters own fingers cutting and pasting but a person who is actually doing something and working towards something, you ignore. Par for the course.
People should summize what the article states. If they can not do that then they should not post endless miles of garbage postings that have nothing to do with our disease.
If they can not summize and then place a link..then they have not got a friggin clue to what they are posting. Summize and tell how it relates to this disease. Why is that so hard to do!??
If not...... people out there..........recognize it as DISINFORMATION CLUTTER! Cuz that what it is!
TRUTH plain and simple..just disinformation and tons of it!
What are any of you actually DOING..DOING to help?
Anyone doing a fundraiser for research? Anyone getting a grant written? Anyone trying to get REAL scientist to help? Anyone doing anything at all??Oh yeah... they say we are doing stuff but we don't have to tell you !
How mature is that. How HS is that? It just states that you are doing nothing at all. Very easy to see right through that one!
This is not YOUR disease, your private disease.....just like AIDS and CANCER and MS....if you are doing something share with the crowd...or are you afraid that the green meanies and men in black will find you and kill you??? EWWWWW! No, better yet make fun of those trying to do something..that is better.
This site is becoming a joke. Endles posts about nothing and no one doing anything..so sad...so very sad!
Now someone maybe is getting publicity by going on that guys show the anti-semite who hates Jews and I guess some press is better than no press but what a person to pick.. a racist anti-semite. OH well...if you can not do any bettter and something is beter than nothing..so I guess it is good. If you hate Jews it is great..I guess. Not many people like that guy so it does hurt us..having him like us...oh well.
If you actually want to do something..call me 434-974-7128 or write email@example.com.
We still need some more reps for more states. Or you can just sit back and complain and try to get a legal thing going about something you can not prove and have not got a grant for or have anyone REAL investigating. It is a joke!
The nuts are running the nut house. G-D help any real research that needs to get done!
Spin your wheels people ....hamsters......or get out of your cage and do something real!
Oh you are but you will not tell me cuz you do not like me......OH yeah..right!
During the End Times, Good will battle Evil. Where do you stand?
Everyone saw that I tried to be nice right?
Funny, I do not consider other peoples posts and thoughts
as garbage like you. I said everyone is valued here.
The only garbage I see posting here comes from you.
That’s why I have no value for you. I gave you a more than
fair chance and you had nothing to back up your allegations.
Nothing!!! All you seem to want to do is b!cth and complain
and dictate what other people should be doing and how wrong
they are for not following your orders.
Talk about London all you wish. Diagnose her with whatever
you feel like diagnosing her with. Chew her up and spit her
out as many times as you like. But the fact remains that as
crazy as you think she is you are considerably worse off with
your narcissist and condescending personality disorder. London
can and will get better, your condition would require a big change
in your personality that would require years of psychotherapy.
FYI it is a fact that Relief seeker is not the first black person I
have heard say that you seem racist, and months before
her observational claims too! This quality seems to
be obviously consistent with you.
Not a good quality to have Randy.
Please be very careful when you live in a glass house.
If you are for real, then I see you trying to find a solution toward
this cause but you just keep shooting yourself in the foot over and
over again because you claim with certainty that you know more
than you honestly do. You cannot even get the victims of this disease
to work with you because of your personality disorder! How on Earth
do you expect to get the help of any state or federal government
agency? How many people here do you think honestly
want you to represent them well intentioned or not?
Take a reality check once in a while. You said people come here to
read your posts. Why then do they not seek your website out?
Why do you lie to yourself? You say this site is a waist of time but
you refuse to leave? Why torture yourself like this? Or us?
Perhaps this disease has you more than you think. I have heard it
said that when the skin symptoms subside this will hit some
people internally even worse; we all know it affects the brain.
Please get this checked with your doctor as I am very concerned
Since you seem to think that people here are paranoid because of
some claims of possibly being monitored, care to tell everyone what
you told me on the phone about being followed yourself? Were
you just having a case of paranoia or were you telling me the truth?
Or was that story disinformation? Can’t seem to make up your mind, hu?
You are being hypocritical and spreading disinformation about what
many people have claimed, including yourself. Your games stink!
Now, stop the b!cthing or leave this site for good. You are causing
way more harm than good here. Don’t you have some work to do
for all of us since we are not doing anything? The CDC
probably postponed their investigation because they needed a
break from all of your negativity. Go tell them to “do something”
and stop b!cthing at the choir already.
I have alerted the monitors here about you once more.
Cool it or be banned for good this time.
Hi, my name is Linda and I have had this "condition" for 15 years now. It developed shortly after I had silicone breast implants back in April of 1990. I have had countless tests performed to the tune of several thousand dollars, lost my house, my job, my husband, my car, and my self esteem. Today, I am living on SSI and rarely leave my house. Like most of you, the doctors all called me crazy and delusional, even though my tests showed a "foreign body invasion", amongst other things, yet all the doctors ignored the tests and dismissed me. When I first got my implants, I had a perfect complexion, but after years of lesions, my face is riddled with scars and I have to spackle on the foundation just to face people. My textured implants were actually recalled by the manufacturer, and yet they (McGhan Corp) filed bankruptcy and I was part of a class action settlement groupl who each received a whopping $795.00 check for our injuries. McGhan was a subsidiary of 3M who was later bought out my Union Carbide. Hence, they have continued to manufacture silicone implants without interruption. Meanwhile, my life has practically been destroyed. My family do not know how to deal with and so they just don't. At times, I have felt so hopeless and alone with my despair that I actually tried to kill myself. Then one day, a few months ago, I was surfing the internet, and I somehow stumbled upon this forum. I wasn't even searching for anything to do with my illness, but somehow I came across a link to here, and I was truly astonished and amazed with what I read. Since that day I have a better outlook on life, and I am filled with something I had almost forgotten about ---- HOPE! Yes, I have read every single post from the beginning up to now, and I feel such a kinship and closeness with you people. Even if we never find a cure, just being able to talk to other people like myself, who understand the nightmare, is, well it is a godsent miracle for me.
With that being said, I would like to throw my tiny two cents in about the accusations and arguing that has been going on amongst some of you. I have a strong belief that who ever is responsible for this tragedy, be it the government, corporate entities, or the devil himself, has got to be pleased as punch when they see us fighting amongst ourselves. Because divided we fall, together we stand. Amongst the many, stand the few. Tamtam is right when we says we should unite together, and fight together, as a team, not against each other. That is the evildoers goal to divide and conquer. Please, please I am pleading with everyone to stay focused on our goal, and leave our egos and personal attacks against each other in some other room. Anywhere but here, our little sanctuary, our haven from the conspirators and nonbelievers who have hurt us. This feels like my last and only chance for justice and possibly a cure. Okay, I think I am rambling again. So, I guess I will shut up now and go to bed next to my faithful sweet companion, my dog Joule the whippet. \
Oh one more thing, it's something good, I took Tamtam's advice and used some terramyacin on a bad sore I had on my chin for 4 months and it cleared it up withing a week!!! More tomorrow after I meet with a potential employer for a job!! Yip, maybe things are looking up afterall.
Goodnight all my FWF (friends with fibers) sorry, I have a twisted sense of humor and I can't help my sagittarius personality is showing again. haha
Linda the Lindster
codon blue, Thanks for your upbeat post. I am glad you joined this board having had this for 15 years. I have had it since early 80's and I also know that this becomes a disabling systemic illness.
randy, I think a lot of people on this board are stumped like me and just don't know how to go about organizing and writing the right kind of letters etc. especially trying to explain this infliction without having the correct technical language. That is why I asked tamtam for some kind of written explanation. I wrote to the person at the Canadian morgellons site and asked him to call me. He actually lives in the US and it turns out that I know him. He is returning to Canada in a few months. I will write letters to government and health officials in the near term, however perhaps you could give me some more suggestions.
Sabrina, I appreciate your input.
Yes.......to all those questions.
I'ts not that I (noticed your trying very hard not to use "I") or we don't "have" to tell YOU. It is however a 'choice' based on history.
As far as "we" still needing state reps; are you refering to your state model prodject? How's that going?
How are your sales of Dr. Schwartz's CD and the US distribution of the cream from Germany doing?
"The investigation by the Centers for Disease Control and Prevention has been delayed until early next year while a 12-member task force assembles a plan, including a formal definition of Morgellons and guidelines for how fibers will be collected, CDC spokesman Dan Rutz said. The scientists hope to determine whether it is contagious and if patients are linked by a common exposure, he said. "
"Between 50 and 200 patients will be referred from dermatologists around Los Angeles, chosen because of a concentrated number of cases in the county, Rutz said. The research team will work out of a Veterans Administration hospital in Los Angeles."
http://www.pe.com/localnews/inland/stor ... 88f52.html
Skytroll, will provide links to study from Fla soon.
Who is online
Users browsing this forum: No registered users and 1 guest