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#109
Feb 2, 2013
 
Deflecting Elicitation Attempts

Know what information should not be shared, and be suspicious of people who seek such information. Do not tell people any information they are not authorized to know, to include personal information about you, your family, or your colleagues.

You can politely discourage conversation topics and deflect possible elicitations by:

■Referring them to public sources (websites, press releases)
■Ignoring any question or statement you think is improper and changing the topic
■Deflecting a question with one of your own
■Responding with Why do you ask?
■Giving a nondescript answer
■Stating that you do not know
■Stating that you would have to clear such discussions with your security office
■Stating that you cannot discuss the matter
If you believe someone has tried to elicit information from you, especially about your work, report it to your security officer.

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#110
Feb 2, 2013
 
Well beauty-product companies usually also start with such question as : does your skin look saggy and tired when you wake up...etc.

http://www.raysahelian.com/collagen.html
Direct collagen orally might work for some conditions, but not topically applied.

So the next question is whether stemcells would give a better result. Apparently human growth-hormone would show a disfiguring or maybe even oncogenic result.

So on to plants. And a roller with 450 sharp needles to get the sharkcollagen mixed with elicitated plant-stemcells to the spot.
Well i've seen pictures, and one is iunderlighted and the other overlighted...so i really would not know.

And now we have a new generation of creams.

If i can find a quick powerpoint presentation, we can also understand how epigenomic switch-on and switch-off works.

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#111
Feb 2, 2013
 
With slides.
http://www.cosmeticsandtoiletries.com/formula...

methylation:epi genomic switch off

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#112
Feb 2, 2013
 
And i'm still wondering whether the Ebola virus might be hiding out in a plant. :P

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#113
Feb 2, 2013
 
The process of skin-renewal is started by it being wounded anyway, and is an old technic.
Needles can be upto 3 mm long just to even reach the collagen and three kinds of other fibres, that are just a kind of gel layer under the 'leather-skin'. And really nobody knows whether killing sharks and using their collagen or expensive plant-stemcells actually work when added.
There is no control and the group is usually self-reporting and too small to be representative.

micro-needling
http://owndoc.com/dermarolling/dermarolling-m...

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#114
Feb 2, 2013
 
A SNP is a polymorphic base where the point mutation has persisted in the population. The term point mutation can occur as a one off event in only one individual. Generally, SNP studies look for bases that have greater than a certain minor allele frequency (e.g. 10% of the population have the minor allele) to show that the SNP is informative and exists in several individuals in a population.

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#115
Feb 2, 2013
 
SNP and POINT MUTATION
both are single-nucleotide differences in a DNA sequence
http://www.ornl.gov/sci/techresources/Human_G...

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#116
Feb 2, 2013
 
non-coding sequences

http://bio.sunyorange.edu/updated2/GENETICS/9...

clear interesting read.

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#117
Feb 2, 2013
 
Science Direct article about renaming ERV's

Abstract
The genomes of many species are crowded with repetitive mobile sequences. In the case of endogenous retroviruses (ERVs) there is, for various reasons, considerable confusion regarding names assigned to families/groups of ERVs as well as individual ERV loci. Human ERVs have been studied in greater detail, and naming of HERVs in the scientific literature is somewhat confusing not just to the outsider. Without guidelines, confusion for ERVs in other species will also probably increase if those ERVs are studied in greater detail. Based on previous experience, this review highlights some of the problems when naming and classifying ERVs, and provides some guidance for detecting and characterizing ERV sequences. Because of the close relationship between ERVs and exogenous retroviruses (XRVs) it is reasonable to reconcile their classification with that of XRVs. We here argue that classification should be based on a combination of similarity, structural features,(inferred) function, and previous nomenclature. Because the RepBase system is widely employed in genome annotation, RepBase designations should be considered in further taxonomic efforts. To lay a foundation for a phylogenetically based taxonomy, further analyses of ERVs in many hosts are needed. A dedicated, permanent, international consortium would best be suited to integrate and communicate our current and future knowledge on repetitive, mobile elements in general to the scientific community.

Abbreviations
dUTPase, deoxyUridineTriPhosphatase; ERV, Endogenous Retrovirus; HERV, Human Endognous Retovirus; HML, Human MMTV like; ICTV, International Committee on the Taxonomy of Viruses; LTR, Long Terminal Repeat; MMTV, Mouse Mammary Tumor Virus; TE, Transposable Element; TSD, Target Site Duplication; XRV, Exogenous Retrovirus
Keywords
Endogenous retrovirus; Taxonomy; Nomenclature; Phylogeny

----------

Figures and tables from this article:

Fig. 1. A. Use of similarity matrices for classification. B. The tendency of younger integrations to occur in tighter subclusters within clusters is shown. Such internal group inhomogeneities were seen during work with HERV-W/ERV9 (Oja et al., 2005), HERV-H (29 and 28), and ERV3/HERV-E sequences (Andersson et al., 2005). When there is drift within a group over a long time period, with successive integrations, the desired simple triangular pattern will be replaced by a series of overlapping triangles, with the oldest integrations (highest LTR divergence) representing a fringe. Group C had a discontinuous integration history, with a recent burst of integrations.
Figure optionsView in workspace
Fig. 2. General strategy for grouping ERVs. The importance of grouping ERVs at levels higher than the host species is emphasized.
Figure optionsView in workspace
Fig. 3. The effect of postintegrational mutation to widen ERV groups, until they are no more discernible by sequence similarity. An approximate limit of 200 million years for similarity based recognition of randomly mutated sequences is indicated. Sets of older integrations will tend to be artificially split into several groups if a fixed degree of similarity, for example a 80% Pol similarity group classification criterion, is used. Such artificial splits can be counteracted by comparing consensus sequences of all ERV groups within the host species, and joining groups which give highly similar consensuses. The situation is the same as for any non-functional transposon (see e.g. Batzer et al., 1996). Mya = million years ago.
Figure optionsView in workspace
Corresponding author. Tel.:+46 18 611 55 93; fax:+46 18 55 10 12.
Copyright 2009 Elsevier B.V. All rights reserved.

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#118
Feb 3, 2013
 
Bibliographic information
This article belongs to a special issue
Genomic Impact of Eukaryotic Transposable Elements
Edited By Jerzy Jurka
Other articles from this special issue

The adaptive role of transposable elements in the Drosophila genomeJosefa Gonzlez , Dmitri A. Petrov
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Endogenous retroviral LTRs as promoters for human genes: A critical assessmentCarla J. Cohen , Wynne M. Lock , Dixie L. Mager
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CloseCarla J. Cohen , Wynne M. Lock , Dixie L. MagerEndogenous retroviral LTRs as promoters for human genes: A critical assessmentGene, Volume 448, Issue 2, 15 December 2009, Pages 105114Review ArticlePDF (370 K).

Genomic Impact of Eukaryotic Transposable Elements, Pacific Grove, California, February 610, 2009Jerzy Jurka
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CloseJerzy JurkaGenomic Impact of Eukaryotic Transposable Elements, Pacific Grove, California, February 610, 2009Gene, Volume 448, Issue 2, 15 December 2009, Pages 103PDF (88 K).
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#119
Feb 3, 2013
 
http://rationalwiki.org/wiki/Common_descent

good summation, clarifies terms and into what relation they stand to common descent.

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#120
Feb 4, 2013
 
percent similarities in genomes and how to calculate them.

Found a doc. Usually it is all done by computer, for that you will finds thousands of sites.

Calculating Community Overlap and Diversity Indices.
https://docs.google.com/viewer...

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#121
Feb 5, 2013
 
About a insulin related hormoon that bodybuilders really dig. PGC-1- alpha
As well as effects on emhanced mitochondria, glycogene, cancer, fybromyalgia, diabetis II and Alzheimer (and not to forget that it mainly enhances the uptake of estrogen-> and therefore it works ;)

A study on human muscle-tissue, with different diets.

http://jap.physiology.org/content/105/4/1098....

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#122
Feb 5, 2013
 
Vitamin C hampering the effects of PGC-1-alpha a.o..
(endurance is studied) I mention it here because the use of anti-oxidants is widely (rather wildly) promoted in cancer patients.

http://ajcn.nutrition.org/content/87/1/142.ab...

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#123
Feb 5, 2013
 
http://www.sciencedaily.com/releases/2010/10/...
A claim by frankly the pharmaceutical industry of having found an Alzheimer/diabetis gene.
Well they did not.
And a the hyped possibilities of a miracle cure.

After a lot of study and searches the socalled gene turns out to be PGC-1-alpha the precursor for estrogen uptake.

quote:
"Our research is the first to find that PGC-1 is a common denominator between Type 2 diabetes and Alzheimer's disease," said Dr. Pasinetti. "This discovery will have significant implications for the more than five million Americans affected by Alzheimer's disease, a number that is expected to skyrocket in the next three decades as the population ages. We look forward to continuing to research this discovery and translate it into the development of novel approaches for disease prevention and treatment."

Dr. Pasinetti and his colleagues are optimistic that if they find that PGC-1 can be manipulated pharmacologically to prevent BACE accumulation in the brain, these studies will provide important insights for the formulation of novel treatments and possible preventative strategies in Alzheimer's disease.

end quote

The next questions to asks is how would this work.

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#124
Feb 5, 2013
 
Let's see what is involved:

The process by which a linear sequence of amino acids folds into a discrete and functional three-dimensional protein is one on which life depends. Although the code that governs folding remains a mystery, we do know that the primary sequence is subject to evolutionary pressure to adjust folding rate and product stability according to physiological needs. The failure of a protein to fold correctly leads to a functional deficit, which can have serious consequences, as in cystic fibrosis. However, there is an emerging class of late-onset, slow-progressing diseases that appear to result instead from a gain of function associated with the abnormally folded form of the protein. These diseases, which are characterized by ordered, fibrillar aggregates comprising different proteins, include common neurodegenerative diseases such as Alzheimers disease (AD) and Parkinsons disease (PD) as well as many rare systemic diseases such as familial amyloid polyneuropathy (1, 2).

What do the fibrillizing proteins have in common? Although all of the fibrils share some morphological features (36), examination of the primary sequences of the constituent proteins does not reveal a conserved motif. In fact, the ability to form fibrils in vitro is not limited to the disease-associated proteins, as illustrated by the paper of Chiti et al. in this issue of the Proceedings (7) and an earlier paper from the same group (8).

>>>> Thus two globular proteins with no homology to the disease-associated proteins or to each other have the ability to form fibrils that resemble those extracted from diseased tissue. In both cases, the globular proteins are prone to fibril formation under conditions that stabilize a partially folded structured form of the protein. Most proteins appear to have evolved to fold without populating such an intermediate (9).<<<<<

The rationale for this phenomenon and its possible implications for degenerative disease will be discussed.
---
So the protein does not fold open properly. Also thought to be the culprit for AAT fibromyalgia. A form that is linked closely to cystic fibrosis.

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#125
Feb 5, 2013
 
cont.

All amyloid fibrils contain beta &#946;-sheet structure in which the peptide strands are aligned orthogonal to the direction of fibril growth (1). This cross-&#946;beta motif may be responsible for the similar widths of most fibrils;

* Link:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3 ...

In contrast, the sequences of fibrillizing proteins are not subject to evolutionary pressure to optimize the fibril or its assembly, but merely to avoid sequences that would lead to juvenile-onset diseases that could interfere with reproduction. Thus, only mutations that promote very rapid fibrillization and possibly, juvenile-onset disease, would be selected against.

TYPE II, by a slightly different process.

Transthyretin, alpha&#945;-synuclein, and the type II diabetes-linked islet amyloid polypeptide all form morphologically similar species (6, 16, 30).

Several studies have demonstrated that genes involved in placentation have evolved adaptively during mammalian descent [2125]. Adaptive evolution can be measured by comparing the per site rates of nonsynonymous (dN) to synonymous (dS) substitutions in protein coding sequences. The ratio of these substitution classes is called dN/dS or w. The values = 1, >1, and <1, are [20]interpreted as signifying neutral evolution, positive selection, and purifying selection, respectively [26]. dN/dS can be measured in a variety of ways [27], but most studies that measure dN/dS are designed to test for evidence of positive selection on particular evolutionary lineages.

quote from science daily:
colleagues found that a gene known as proliferator-activated receptor coactivator 1 (PGC-1), a key regulator of glucose currently investigated as a potential therapeutic target for Type 2 diabetes, is decreased in Alzheimer's disease. The team reports that this decrease might be causally linked to promotion of Alzheimer's disease. They found that PGC-1 promotes degradation of a specific enzyme known as beta-secretase (BACE). ACE is directly involved in the processing and eventually generation of &#946;-amyloid, an abnormal protein highly linked to Alzheimer's disease and brain degeneration.

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#126
Feb 5, 2013
 
*Link:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3...
Proc Natl Acad Sci U S A. 1999 March 30; 96(7): 33423344. PMCID: PMC34271
Evolution of amyloid: What normal protein folding may tell us about fibrillogenesis and disease
Peter T. Lansbury, Jr.*
Center for Neurologic Diseases, Brigham and Womens Hospital, Department of Neurology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115*To whom reprint requests should be addressed. e-mail: lansbury@cnd.bwh.harvard.edu.

Copyright 1999, The National Academy of Sciences
See the article"Designing conditions for in vitro formation of amyloid protofilaments and fibrils" on page 3590.
This article has been cited by other articles in PMC.

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#128
Feb 5, 2013
 
cont.

Alzheimer and Diab. II are basicly about a proteine-lipid interaction.

http://www.ncbi.nlm.nih.gov/pubmed/15182369

APP undergoes rapid anterograde transport in neurons. During its transport, APP was found to interact with kinesin-I and functions as a kinesin-I membrane receptor to mediate axonal transport of beta&#946;-secretase (BACE1) and PS1 [26,27]. However, another study failed to verify the interaction between APP and kinesin-I and the co-transport of BACE1 and PS1 with APP [28]. We recently found that APP and its derived membrane-associated form, CTFs, can regulate cell surface delivery of PS1/gamma&#947;-secretase but not BACE1 [29]. In addition, APP was found to be a major component of herpes simplex viral particles and likely mediates fast anterograde transport of these particles [30,31]. Another study showed that increased doses of APP markedly decreased retrograde transport of nerve growth factor and resulted in degeneration of forebrain cholinergic neurons in a mouse model of Down's Syndrome [32]. APP was also found to interact with high-affinity choline transporter (CHT) through the C-terminal domain and APP deficiency affected CHT endocytosis [33]. Overall, most studies suggest that APP plays some role in regulating protein trafficking.

Molecular Brain APP Processing in Alzheimer.
The APP gene is found on chromosome 21.
http://www.molecularbrain.com/content/4/1/3
beta ACE stands for splicing APP.

--- So the point would be acidification.
I would simply stay away from High Fructose Corn Sugar and all corn-sirup products. Made from corn/mais, and added to just about all pre-prepared food and sweets, cereals a.s.o.
They have the same detrimental effect on the brain.->acidification that interrupts neural growth and connectivity.
And makes the body fat real fast.

If you wanted to duplicate the effects of DIAB.II and Alzheimer, you could not find a better way.

IF APP is frankly a regulating mechanism (closely related hormonal enzym to insulin, that can in high dosage give rats anorexia.), it will try to counteract all the excess, but in doing so attracts co-location of proteins with fiber-proteins, or the toxic phase just before that.
And the key is probably hiding in the RNA.

So we also find methylation.
And hormonal Alzheimer caused by an epigenetic, phenotypical disturbance that the body is not capable of dealing with.
Or environmental cocktails of toxins.

PGC-1
A proliferator-activated receptor gamma coactivator-1
Short name: PGC-1 beta
or PPAR-gamma activator-1 beta
or PPARGC-1-beta

ALTERNATIVE MAME(S): PGC-1 RELATED ESTROGEN RECEPTOR
PGC-1- alpha has the same effect, but is also sold as a proteine to enhance muscles or stimulate bone repair.

(And i'm making this post to find out if it is allready i some form on the market. The quantities used in studies are franly over the top. And only in purified injectables. Or as IGF from antlers.)

So it's estrogen, the pill, or rather a combination, a boost so to say, but sold as a fancy gen, or expensive protein and I'll bet even more expensive medication.

So you can look for the protein pgc-1-alpha and it's price and take estrogen, and leave those HFCS High Fructose Corn/mais Sugars alone and add more f.i. lentils or linseed (cheap option) or nuts(ALA, just as good and precursor to the good fish oils) and fish to your diet.
Green tea EGCG, like exercise, boosts SIRT-1 a precursor to PGC-1-alpha.
SIRT usually degrades quickly (also with resveratrol) but less quick with green tea extract.
And do loose weight.

'Irisin' is a term you might also find related to this topic. But googling is not effective. It relates to messenger RNA involved in the PGC-1A process.

The next things to look in are CAMP and the proteine locking/binding to nucleate receptor type 2.

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#129
Feb 5, 2013
 
http://www.nature.com/nature/journal/v481/n73...

A PGC1-&#945;-dependent myokine that drives brown-fat-like development of white fat and thermogenesis
Pontus Bostrm,1 Jun Wu,1 Mark P. Jedrychowski,2 Anisha Korde,1 Li Ye,1 James C. Lo,1 Kyle A. Rasbach,1 Elisabeth Almer Bostrm,3 Jang Hyun Choi,1 Jonathan Z. Long,1 Shingo Kajimura,4 Maria Cristina Zingaretti,5 Birgitte F. Vind,6 Hua Tu,7 Saverio Cinti,5 Kurt Hjlund,6 Steven P. Gygi2 & Bruce M. Spiegelman1

Abstract.

Exercise benefits a variety of organ systems in mammals, and some of the best-recognized effects of exercise on muscle are mediated by the transcriptional co-activator PPAR-&#947; co-activator-1 &#945; (PGC1-&#945;). Here we show in mouse that PGC1-&#945; expression in muscle stimulates an increase in expression of FNDC5, a membrane protein that is cleaved and secreted as a newly identified hormone, irisin. Irisin acts on white adipose cells in culture and in vivo to stimulate UCP1 expression and a broad program of brown-fat-like development. Irisin is induced with exercise in mice and humans, and mildly increased irisin levels in the blood cause an increase in energy expenditure in mice with no changes in movement or food intake. This results in improvements in obesity and glucose homeostasis. Irisin could be therapeutic for human metabolic disease and other disorders that are improved with exercise.

11.january.2012

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