Human Anatomy, Physiology, and Medicine. Anything human!
In this article on cloaking protein, is the promoter the catalyst? It seems there is a cloaking of unknown protein.
How malaria dupes immune system
The majority of deaths from malaria are among under-fives
Scientists have discovered the genetic secret behind the ability of the malaria parasite to evade attack by the human immune system.
They have shown how it can turn on and off genes that manufacture a series of 'cloaking' proteins used as camouflage.
If one protein is recognised by the immune system, the parasite simply produces another type.
The study, by Howard Hughes Medical Institute researchers based in Australia, is published in Nature.
How can it turn on and off? by the signal? How can the parasite just produce another type of protein if it is not programmed to switch by signal. What would that signal be?
Every answer represents a type research.
The "only thing" to be presented for the time being is a survey.
More video footage will be made available next month.
You all can be helpfull to get the video link -preferably- on international message boards
(with or without introduction or translation)
Histone H2A variants H2AX and H2AZ
Christophe Redon, Duane Pilch, Emmy Rogakou*, Olga Sedelnikova,
Kenneth Newrock and William Bonner
Two of the nucleosomal histone families, H3 and H2A, have
highly conserved variants with specialized functions. Recent
studies have begun to elucidate the roles of two of the H2A
variants, H2AX and H2AZ. H2AX is phosphorylated on a
serine four residues from the carboxyl terminus in response to
the introduction of DNA double-strand breaks, whether these
breaks are a result of environmental insult, metabolic mistake,
or programmed process. H2AZ appears to alter nucleosome
stability, is partially redundant with nucleosome remodeling
complexes, and is involved in transcriptional control.
Laboratory of Molecular Pharmacology, Center for Cancer Research,
Feedback please. I will help you, please be more specific with your directions OR what you want said. I know of many message boards-Okay, nevermind explaining...I just re-read your request.
The Flowers By The Sea
When over the flowery sharp pasture's
edge, unseen, the salt ocean
lifts its form - chicory and daisies
tied, released, seem hardly flowers alone
but, color and the movement - or the shape
perhaps - of restlessness, whereas
the sea is circled and sways
peacefully upon its plant-like stem
Last edited by Skytroll on Sat Jan 14, 2006 4:11 pm, edited 1 time in total.
The trichothecene mycotoxins are a diverse group of more than 40 compounds produced by fungi. They are potent inhibitors of protein synthesis, impair DNA synthesis, alter cell membrane structure and function, and inhibit mitochondrial respiration. Sec ondary metabolizes of fungi, such as T-2 toxin and others, produce toxic reactions called mycotoxicoses upon inhalation or consumption of contaminated food products by humans or animals. Naturally occurring trichothecenes have been identified in agricultu ral products and have been implicated in a disease of animals known as moldy corn toxicosis or poisoning.
There are no well-documented cases of clinical exposure of humans to trichothecenes. However, strong circumstantial evidence has associated these toxins with alimentary toxic aleukia (ATA), the fatal epidemic seen in Russia during World War II, and wit h alleged BW incidents ("yellow rain") in Cambodia, Laos and Afghanistan.
Consumption of these mycotoxins results in weight loss, vomiting, skin inflammation, bloody diarrhea, diffuse hemorrhage, and possibly death. The onset of illness following acute exposure to T-2 (IV or inhalation) occurs in hours, resulting in the rapi d onset of circulatory shock characterized by reduced cardiac output, arterial hypotension, lactic acidosis and death within 12 hours.
Clinical signs and symptoms of ATA were hemorrhage, leukopenia, ulcerative pharyngitis, and depletion of bone marrow. The purported use of T-2 as a BW agent resulted in an acute exposure via inhalation and/or dermal routes, as well as oral exposure upo n consumption of contaminated food products and water. Alleged victims reported painful skin lesions, lightheadedness, dyspnea, and a rapid onset of hemomhage, incapacitation and death. Survivors developed a radiation-like sickness including fever, nausea , vomiting, diarrhea, leukopenia, bleeding, and sepsis.
Specific diagnostic modalities are limited to reference laboratories. Because of their long "half-life" the toxin metabolizes can be detected as late as 28 days after exposure.
General supportive measures are used to alleviate acute T-2 toxicoses. Prompt (within 5-60 min of exposure) soap and water wash significantly reduces the development of the localized destructive, cutaneous effects of the toxin. After oral exposure mana gement should include standard therapy for poison ingestion.
Ascorbic acid (400-1200 mg/kg, inter-peritoneal (ip)) works to decrease lethality in animal studies, but has not been tested in humans. While not yet available for humans, administration of large doses of monoclinal antibodies directed against T-2 and metabolizes have shown prophylactic and therapeutic efficacy in animal models.
Thanks for the extended posts on Quorum sensing...makes more sense now in relation
to what I understand so far about this. Thank you.
I think TamTam was just asking for help spreading awareness of the video.
Take a break by all means. But this forum needs you.
Nature. 2001 Nov 8;414(6860):160-1.
Identification of the cellular receptor for anthrax toxin.
Bradley KA, Mogridge J, Mourez M, Collier RJ, Young JA.
McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, 1400 University Avenue, Madison, Wisconsin 53706, USA.
The tripartite toxin secreted by Bacillus anthracis, the causative agent of anthrax, helps the bacterium evade the immune system and can kill the host during a systemic infection. Two components of the toxin enzymatically modify substrates within the cytosol of mammalian cells: oedema factor (OF) is an adenylate cyclase that impairs host defences through a variety of mechanisms including inhibiting phagocytosis; lethal factor (LF) is a zinc-dependent protease that cleaves mitogen-activated protein kinase kinase and causes lysis of macrophages. Protective antigen (PA), the third component, binds to a cellular receptor and mediates delivery of the enzymatic components to the cytosol. Here we describe the cloning of the human PA receptor using a genetic complementation approach. The receptor, termed ATR (anthrax toxin receptor), is a type I membrane protein with an extracellular von Willebrand factor A domain that binds directly to PA. In addition, a soluble version of this domain can protect cells from the action of the toxin.
*****I just read about Von Williebrand factor today. I believe it is where one's blood will not clot?
You can not discuss laboratory results before multiple test are run.
Because this target represents a multi cellular like entity
the process - and its interaction- is complex.
Answers are research budget depending.
This includes much time.
The best support you can give is to send the link out to international message boards.
A Spanish introduction would be welcome and not to forget all other languages.
As soon as the matter will get more attention the Institutes will go after it.
In fact they already do.
So, be ingenious.
tamtam may consider to patent london's nose as a broad spectrum bio sensor.
Reference: cyanobacterium/ blue green algae/ cystic fibrosis
[PDF] Georg Nagel The cystic fibrosis chloride channel Channelrhodopsins
File Format: PDF/Adobe Acrobat
hereditary disease Cystic Fibrosis (“Mukoviszidose”). We express ... Channelrhodopsins:
Green algae were postulated to contain micro- ...
http://www.mpibp-frankfurt.mpg.de/nagel/nagel.pdf - Similar pages
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