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Post by lilsissy on Jul 31, 2012 11:25:36 GMT -5
SEARCH GOOGLE QUERY YAC B129B12 fiber results below, artificial - BioMedSearch www.biomedsearch.com/searchlist.html?p=149&query_txt... Results 7401 - 7450 of 282163 – ... transplantation with a novel wound dressing based on artificial hollow fiber membrane capillaries. ..... YAC B129B12 is 120 kb . Publications by Author L D Griffin | AbstractBoard.com www.abstractboard.com/author/Griffin+L+D/L-D-Griffin.htmlPolarized light imaging (PLI) is a method to image fiber orientation in gross ...... YAC B129B12 is 120 kb in length and maps entirely to chromosome 10.
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Post by lilsissy on Jul 31, 2012 11:30:18 GMT -5
This is for another thread but this is good , very good to note Self-organizing high-order cognitive functions in artificial agents: Implications for possible prefrontal cortex mechanisms. Ads by Google LPN to RN Bridge Programs RN/ADN Degree Online, 12-18 Months. NLN Accredited School No Wait List. www.CollegeNetwork.com/LPN2RN MedLine Citation: PMID: 22609533 Owner: NLM Status: Publisher Abstract/OtherAbstract: In our daily life, we often adapt plans and behaviors according to dynamically changing world circumstances, selecting activities that make us feel more confident about the future. In this adaptation, the prefrontal cortex (PFC) is believed to have an important role, applying executive control on other cognitive processes to achieve context switching and confidence monitoring; however, many questions remain open regarding the nature of neural processes supporting executive control. The current work explores possible mechanisms of this high-order cognitive function, transferring executing control in the domain of artificial cognitive systems. In particular, we study the self-organization of artificial neural networks accomplishing a robotic rule-switching task analogous to the Wisconsin Card Sorting Test. The obtained results show that behavioral rules may be encoded in neuro-dynamic attractors, with their geometric arrangements in phase space affecting the shaping of confidence. Analysis of the emergent dynamical structures suggests possible explanations of the interactions of high-level and low-level processes in the real brain.
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Post by lilsissy on Jul 31, 2012 11:53:02 GMT -5
Well never really looked at this new DX arthritis.webmd.com/tc/ankylosing-spondylitis-topic-overviewbut again here as I have suspected is the HLA-B-27 Causes of Ankylosing Spondylitis Although the exact cause of AS is unknown, we do know that genetics play a key role in AS. Most individuals who have AS also have a gene that produces a "genetic marker" - in this case, a protein - called HLA-B27. This marker is found in over 95% of people in the Caucasian population with AS (the association between ankylosing spondylitis and HLA-B27 varies greatly between ethnic and racial groups, see our AS Diagnosis section for more information). It is important to note, however, that you do not have to be HLA-B27 positive to have AS. Also, a majority of the people with this marker never contract ankylosing spondylitis. Scientists suspect that other genes, along with a triggering environmental factor, such as a bacterial infection, are needed to trigger AS in susceptible people. HLA-B27 probably accounts for about 40% of the overall risk, but then there are other genes working in concert with B27. There are probably five or six genes involved in susceptibility toward AS. It is thought that perhaps AS starts when the defenses of the intestines start breaking down and bacteria from the intestines pass into the bloodstream directly into the region where the sacroiliac joints are located.
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Post by lilsissy on Jul 31, 2012 12:00:48 GMT -5
The stiffening of the chest can feel like the discomfort or "heaviness" of a heart attack. Ankylosing spondylitis can also cause the heart to work less efficiently.
If you have any symptoms of heart or lung problems-including heaviness of the chest or pain with deep breathing-talk to a doctor right away to make sure you don't have any serious heart or lung problems. For more information on heart and lung problems, see the topics Heart Attack and Unstable Angina and Pleurisy.
Ankylosing spondylitis is one disease in a group of joint diseases called the spondyloarthropathies (say "spon-dill-o-ar-THROP-a-thees"). These include psoriatic arthritis, reactive arthritis (Reiter's syndrome), and enteropathic arthritis (joint problems linked with inflammatory bowel disease). Although inflammation of the spine also occurs in these other conditions, it is less common and less severe than the inflammation that occurs in ankylosing spondylitis. end cut
the bowel
this artificial goes through it.
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Post by lilsissy on Jul 31, 2012 12:23:12 GMT -5
So HLA 2 POSTIVE goes with the artificial here, HLA-Ig Based Artificial Antigen Presenting Cells for Efficient ex vivo Expansion of Human CTL to magnetic dynobeads www.jove.com/video/2801/hla-ig-based-artificial-antigen-presenting-cells-for-efficient-exCite this Article Chiu, Y., Schneck, J. P., Oelke, M. HLA-Ig Based Artificial Antigen Presenting Cells for Efficient ex vivo Expansion of Human CTL. J. Vis. Exp. (50), e2801, DOI: 10.3791/2801 (2011). Abstract CTL with optimal effector function play critical roles in mediating protection against various intracellular infections and cancer. However, individuals may exhibit suppressive immune microenvironment and, in contrast to activating CTL, their autologous antigen presenting cells may tend to tolerize or anergize antigen specific CTL. As a result, although still in the experimental phase, CTL-based adoptive immunotherapy has evolved to become a promising treatment for various diseases such as cancer and virus infections. In initial experiments ex vivo expanded CMV (cytomegalovirus) specific CTL have been used for treatment of CMV infection in immunocompromised allogeneic bone marrow transplant patients. While it is common to have life-threatening CMV viremia in these patients, none of the patients receiving expanded CTL develop CMV related illness, implying the anti-CMV immunity is established by the adoptively transferred CTL1. Promising results have also been observed for melanoma and may be extended to other types of cancer2. While there are many ways to ex vivo stimulate and expand human CTL, current approaches are restricted by the cost and technical limitations. For example, the current gold standard is based on the use of autologous DC. This requires each patient to donate a significant number of leukocytes and is also very expensive and laborious. Moreover, detailed in vitro characterization of DC expanded CTL has revealed that these have only suboptimal effector function 3. Here we present a highly efficient aAPC based system for ex vivo expansion of human CMV specific CTL for adoptive immunotherapy (Figure 1). The aAPC were made by coupling cell sized magnetic beads with human HLA-A2-Ig dimer and anti-CD28mAb4. Once aAPC are made, they can be loaded with various peptides of interest, and remain functional for months. In this report, aAPC were loaded with a dominant peptide from CMV, pp65 (NLVPMVATV). After culturing purified human CD8+ CTL from a healthy donor with aAPC for one week, CMV specific CTL can be increased dramatically in specificity up to 98% (Figure 2) and amplified more than 10,000 fold. If more CMV-specific CTL are required, further expansion can be easily achieved by repetitive stimulation with aAPC. Phenotypic and functional characterization shows these expanded cells have an effector-memory phenotype and make significant amounts of both TNFá and IFNã (Figure 3).
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Post by lilsissy on Jul 31, 2012 12:30:25 GMT -5
learning, In humans, MHC is also called human leukocyte antigen (HLA). MHC gene families are found in all vertebrates, though they vary widely, chickens having among the smallest known MHC regions (19 genes). In humans the MHC region occurs on chromosome 6, between the flanking genetic markers MOG and COL11A2, and contains 140 genes spanning 3.6 mega base pairs (3.6 Mb or 3 600 000 bits).[2] About half have known immune functions. The same markers in the gray short-tailed opossum (Monodelphis domestica), a marsupial, span 3.95 Mb yielding 114 genes, 87 shared with humans.[3] Marsupial MHC genotypic variation lies between eutherian mammals and birds—taken as minimal MHC encoding—but is closer in organization to that of nonmammals, and MHC class I genes of marsupials have amplified within the class II region, yielding a unique class I/II region.[3] Class III function very differently from class I and class II, but its locus occurs between the other two classes—on chromosome 6 in humans—and are frequently discussed together. en.wikipedia.org/wiki/Major_histocompatibility_complexMajor histocompatibility complex (MHC) is a cell surface molecule encoded by a large gene family in all vertebrates. MHC molecules mediate interactions of leukocytes, also called white blood cells (WBCs), which are immune cells, with other leukocytes or body cells. MHC determines compatibility of donors for organ transplant as well as one's susceptibility to an autoimmune disease via crossreacting immunization. In humans, MHC is also called human leukocyte antigen (HLA). Peptides are processed and presented by two classical pathways: In MHC class II phagocytes such as macrophages and immature dendritic cells uptake entities by phagocytosis into phagosomes—though B cells exhibit the more general endocytosis into endosomes—which fuse with lysosomes whose acidic enzymes cleave the uptaken protein into many different peptides. Via physicochemical dynamics in molecular interaction with the particular MHC class II variants borne by the host, encoded in the host's genome, a particular peptide exhibits immunodominance and loads onto MHC class II molecules. These are trafficked to and externalized on the cell surface.[6]
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Post by lilsissy on Jul 31, 2012 12:50:15 GMT -5
Interesting sexual selection tied to ..... a cluster of genes on chromosome 6 at loci 6p21. All living cells have structures called antigens present on their cell surface. Antigens are either a polysaccharide or a protein that reacts specifically with a cell surface receptor or an antibody. For each person and each type of cell there are different antigens on the cell’s surface. The unique, genetically-determined antigens present on cell surfaces are determined by a cluster of genes on chromosome 6 at loci 6p21.3 en.wikipedia.org/wiki/Major_Histocompatibility_Complex_and_Sexual_SelectionGenesis 6.6
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Post by lilsissy on Jul 31, 2012 13:06:19 GMT -5
www.hindawi.com/journals/cdi/2012/584374/hmmmm.. Evolution of MHC genes and alleles is driven by the need to maximize peptide binding diversity in order to recognize a maximum of potential pathogens. Polymorphism and polygeny are two (independent) genetic mechanisms for increasing variety of MHC class I and class II proteins. Polygeny acts on the individual level, whereas polymorphism is (primarily) a population-relevant criterion. Thus, a maximum number of class I and II genes would ensure the greatest conceivable protection of a single individual against pathogens. However, polygeny is limited by a mechanism called “MHC restriction”: T cells recognize fragmented antigens (self and foreign) only in conjunction with MHC proteins [42, 67]. To avoid autoimmune reactions, T cells that strongly react with MHC molecules presenting self-peptides are deleted. In consequence of these opposed requirements, the immune surveillance is a delicate balance between self and foreign as well as between (self-)tolerance and immune response. Furthermore, these two opposing demands create a dilemma: On the one hand, many MHC genes would present a maximum of different peptides but on the other hand, the presentation of many different self-antigens would strongly reduce the T cell diversity. Thus, MHC restriction limits T cell antigen recognition and response. As a consequence of this, the diversity of MHC class I and II proteins of a single individual is limited (and optimized) to six different molecules (3 genes × 2 alleles). The optimal number is called “immunogenetic optimum” [68]. Due to the limited number of MHC genes, some agents may evolve polypeptides that evade the immune system of single individuals, but the enormous polymorphism within a population diminishes the possibility that a pathogen can exterminate a whole species (individual C). However, there is a major drawback of this kind of defense strategy: if the size of a population decreases strongly, some MHC haplotypes will disappear, leading to a reduction of MHC diversity, which in turn will negatively affect survival of the population [69]. In summary, the number of different MHC genes is a delicate balance between the key requirement of an entire population/species and the core requests of its individuals.
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Post by lilsissy on Jul 31, 2012 13:33:14 GMT -5
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Post by skyship on Jul 31, 2012 16:54:50 GMT -5
Due to the limited number of MHC genes, some agents may evolve polypeptides that evade the immune system of single individuals, but the enormous polymorphism within a population diminishes the possibility that a pathogen can exterminate a whole species (individual C). However, there is a major drawback of this kind of defense strategy: if the size of a population decreases strongly, some MHC haplotypes will disappear, leading to a reduction of MHC diversity, which in turn will negatively affect survival of the population [69]. In summary, the number of different MHC genes is a delicate balance between the key requirement of an entire population/species and the core requests of its individuals. www.hindawi.com/journals/cdi/2012/584374/========================= from your link Lil Sis, this is what I mean. This is how this can be used for pop studies. Certain phenotypes and haplotypes are created by using certain genes on certain humans. I think it is specific, in otherwords, some are selected for the test. It is a test> Just like Job. But, it can eliminate certain genetic types, or haplotypes, why the mitochondria is so important, it removes or replaces our given mito for another type. Which can either help or hinder us depending on our X chromosomes and what is in our specific genes. Using evolution to devolve some, and sometimes, I feel I am turning to stone, physically. Skin callouses and then hardens and melanin is gone. So, these forms eat melanin somehow. Your skin keeps getting white spots where melanin is lost. melanin is in the S. cereviscaea yeast which is core to the YAC. Yeast artificial chromosome, and this is replacing our histones on I bel. 3 and 4. So, it can be what is devouring the melanin, since that is what it recognizes.
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Post by skyship on Jul 31, 2012 17:43:26 GMT -5
They say life began in the sea.
However using algae to sink CO2 could be the issue. These algae blooms are dangerous and stay on surface for a long time, If they sink carbon what does it grow in the ocean.?
You said:
"the ocean...the dead zones now grow new type bacteria that break down artificial polymers so if they are growing artificial polymers in us and we come in contact with this new type nylon eating bug...it would break down the artificial in us....what % are we now artificial?
The Oceans are filled with the knowledge of mankind...Oceans of man....and I stood upon the sands of the SEA"
you know what I am think is the BM....the bone morphogenic forms......... the scoliosis, part and Shermans disease seem to involve gall stones, kidney stones pancreatic particulate matter. or calculini they call it. If the ascites died, they callous and form calcium deposits or uracil deposits?
mmmmmmm
So these would artificial forms, but, they can be made of organic materials. The crossover, the pearl, the shells of things, the hooves, the bone, calcium phosphorus, potassium uracil .....?
this is so involved.
skyship
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Post by skyship on Jul 31, 2012 19:08:04 GMT -5
origin of natural uracil: Uracil is a common and naturally occurring pyrimidine derivative.[2] Originally discovered in 1900, it was isolated by hydrolysis of yeast nuclein that was found in bovine thymus and spleen, herring sperm, and wheat germ.[3] It is a planar, unsaturated compound that has the ability to absorb light.[4] So, there is the "spark of life" the light?" Studies reported in 2008, based on 12C/13C isotopic ratios of organic compounds found in the Murchison meteorite, suggested that uracil, xanthine and related molecules were formed extraterrestrially.".....en.wikipedia.org/wiki/Uracil_nucleotides========== Some how the change was done through the RNA with uracil way back. Until they found it is radioactive? Or is it really?
============ this makes me think that a meteorite was involved in the Moses saga. They said to collect the manna or dew in the am, at certain times. Why? Because it was in pure form as meteorite passed but left the particles. So what would this have to do with uracil? Was uracil really "Star dust"? the real?
But an artificial form was created.??
pyrimidine derivitive? \============== Methylation of uracil produces thymine. In DNA, the evolutionary substitution of uracil for thymine may have increased DNA stability and improved the efficiency of DNA replication. Uracil can base-pair with any of the bases, but readily pairs with adenine because the methyl group is repelled into a fixed position.Uracil pairs with adenine through hydrogen bonding. Uracil is the hydrogen bond acceptor and can form two hydrogen bonds. In RNA, uracil binds with a ribose sugar to form the ribonucleoside uridine. When a phosphate attaches to uridine, uridine 5'-monophosphate is produced.=================== this ribose sugar binds with uracil in RNA forms Ribonucleoside not tide.......uridine. So the phosphate added makes: 5'monophosphate? monophosphate? so one unit of phosphate and sugar? oligonucleoside??? same as PEG? Now we have the artificial strand and they make more carriers.Delayed release oral pharmaceutical formulations and methods for enhanced intestinal drug absorption. The formulation comprises a first population of carrier particles comprising a drug and a penetration enhancer which are released at a first location in the intestine, and a second population of carrier particles comprising a penetration enhancer and a delayed release coating or matrix. This penetration enhancer is released at a second location in the intestine downstream from the first location and enhances absorption of the drug when it reaches the second location. www.freepatentsonline.com/y2005/0196443.htmlSo, these carriers move around the intestine but make a matrix. do they ever leave the body? ARe they expelled out with the cellulose it breaks down. I don't think so. I think they can permeate the intestinal cell wall and any other cell.
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Post by skyship on Jul 31, 2012 19:12:05 GMT -5
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thelma
Junior Member
Posts: 82
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Post by thelma on Aug 3, 2012 10:15:45 GMT -5
Bump
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