User talk:Pdeitiker

Can you please stop insinuating that all disagreement can be explained my emotional attachment to whatever you think I am attached to? That is in itself uncivil and unconstructive behavior, and not a recommended approach even in cases where it is true.--Andrew Lancaster (talk) 14:15, 17 November 2009 (UTC)

If the shoe fits. Wear it. You own the current problem, it will not be solved until you calm down and stop taking everything so personally. You seem dead-fast on pointing out others errors, but not realizing your complicity to the major problem, areas that you have recently worked on are full of jargon and should be made readable to the common public.PB666 ^yap 20:51, 17 November 2009 (UTC)

I do not have to wear anything. What I am asking you to do is follow Wikipedia policy. I have been trying to discuss particular edits. Interpreting all disagreements as personal attacks, which is what you are doing INSTEAD of good faith editing now, is explicitly an example of uncivil editing according to WP:UNCIVIL.--Andrew Lancaster (talk) 07:21, 18 November 2009 (UTC)

This is a clear example of the black cat calling the kettle black. Andrew. Here is an example of your behavior. What you wrote here is not editing in good faith pb666 going for it. By my standard it is bad faith editing. I asked you to verify the names before altering them. Instead of verifying the names from Redding sources The rs nomemclature is a recognized standard and we have not discussed any "precedent" which says otherwise. however true that may be, that is not what you have been using in your articles, IOW you personally established a precedence, by changing that precedence ad lib may confuse the reader and will make the article more jargonistic. You have not given a good reason yet for changing the name, you are only trying to cover up the fact that you made a possible missassumption about the origin of the name (a page, versus the proper name Page), and I consider this bad faith. We can look at this 2 ways, what I should interpret as good faith, and what is bad faith editing. The title of the section - bad faith, the failure to underscore the precedent you have been using, or the fact you switch nomenclature mid-article and point this as a fault in my understaind of Underhill, bad faith. Was pb666 going fot it, or was he just trying to get you to WP:VERIFY.

I repeat this, you are not going to get me to back off on pushing the readability aspects of the article, I am doing this for your own improvement such that in future you can do this with Y-DNA pages by yourself. I have had the almost same discussions with older editors (3 years back) that you are having with me now. Its about being encyclopedic, you can have all your favorite information in an article (or list) but you must pull from within yourself to make it accessible to others, otherwise for what good reason is it. Science is about 2 aspects:Research and communication. Here is a venue of communication, at some point it may take 5 minutes to create one good sentence, from here on out every sentence will be much more difficult to construct because now it has to make sense at all levels, from the lowest to the highest. I am not your competitor as I told you I really couldn't care less about R1a, OK, its the reader whom you have to be courting.

If you are going to take something and make it more jargonistic, without proper introduction and without graphical explanation, I am going to hold you to the standard, "Why are you doing it?" While I am arguing with you here I could be working on the maps, I could be working in the mtDNA page (which is an interest). While you are arguing with me you could be writing a much more comprehensive lead, improving the readability of the article. PB666 ^yap 14:56, 18 November 2009 (UTC)

I get the picture, and I think you put your finger on the problem you are creating very well: you are trying to teach everyone to do what you prefer; you see your personal preferences, even concerning things you are not good in, to be of a higher rank. You think you do not need to understand the opinions of others. That is the big problem.Andrew Lancaster

I nominated the article for GA status, one of the referees has placed a note on the page saying we need to improve the readability. I am trying to give you advice based on the GA and FA pages I have worked. Andrew its not easy, one editor JFW busted my balls over the edits I introduce. We almost went to arbitration over his insistence that I have a review article verification over something that was midstream in my field of expertise, that I new without doubt was correct. So don't take it personally.

You say "its the reader whom you have to be courting" but in practice you demand that everyone courts you. And you are NOT a typical reader. Let me work on the jargon please. At the moment I have to struggle constantly just to stop your from edits which are designed purely to make a point.

There is a saying, I know what it looks like when I see it, everyone is a great armchair quarterback, but how many of them are actually critiqued. I am singling you out because you want to improve the article, but more importantly if you work hard at it and focus, item by item, you can improve the article. Once you improve this article, you will be much more easily able to improve other articles. However if you keep drawing or waiting for others to step up, it will not get done.

You make a big point above about the "going for it" description. But in fact your own words on talk pages now constantly centre around gung-ho words chosen by you: "I repeat this, you are not going to get me to back off on...". So by your own account you are on a big personal push, and going for it. In contrast, your constant reference to my emotions, starting immediately after I raised concerns with the article split you did, does not have the same excuse: you have never pointed to evidence for the assumptions about my motives which you have made central to your communication with me. I have always explained my preferences in neutral terms, something which you do not even bother to do.--Andrew Lancaster (talk) 15:38, 18 November 2009 (UTC)

The line has to be drawn somewhere, on other pages major contributing editors have done the same thing to me. I am not singling you out. My point is that 90% of the edits at this point need to be directed at making the article more encyclopedic, if you are not familiar you need to review this. I criticize you about your referencing and you blew up in my face, good faith. Click underhill et als Doi: doesn't work, pubmed ID, not present. Tell me, you say you know how to do it, and you wont listen to what I said about how to easily improve the references, and yet the reference you provided does not link. Very unable to accept critique is the way I look at this. Which is more encyclopedic M17 or rs23687894122. How would you like to be called Andrew or ss#987-65-4321? Which is easier for you to read.

By the way, you seem to be saying you can name cases where I have been making the text more "jargonistic" and less accessible. If you are serious about wanting me to fix them can you please point them out so I (and other editors) can look into it? Please do so on the article talkpage. As mentioned many times, I do accept that the article can be improved, and I would like to have the chance to work on that again more than recently.--Andrew Lancaster (talk) 16:10, 18 November 2009 (UTC)

The phylogenetic ("family tree") naming system commonly used for this haplogroup remains inconsistent in different published sources. Although it has not yet used much in published surveys, a more comprehensive survey of the known mutations is listed by ISOGG, and an equivalent tree is given in Underhill et al. (2009) harvcoltxt error: no target: CITEREFUnderhill_et_al.2009 (help).^[1]

Prior to 2009 the mutation SRY1532.2 (or SRY10831.2) defined R1a, and this is also how the term R1a is most often used in publications before 2009.

However the term R1a is also now increasingly used to refer to a broader family including not only this "old" R1a, but also other related R1 (R-M173) lineages which have been found to share several unique mutations with R1a, including M420. In this newer system, the clade defined by SRY1532.2/SRY10831.2 moves from "R1a" to "R1a1".

<--------Starting from this point below I have reworded, not perfect as I said a good correction may take an hour or more to correct--> The family tree of R1a as a whole can be divided into three levels of branching. The following summary is based upon the large survey of Underhill et al. (2009) harvcoltxt error: no target: CITEREFUnderhill_et_al.2009 (help) as follows:

1. R1a* (new nomenclature). Defined as M420 positive but SRY1532.2 negative. (Articles published before the discovery of M420 will not have distinguished these from other R1-M173 lineages.) Underhill et al. (2009) harvcoltxt error: no target: CITEREFUnderhill_et_al.2009 (help) believe this clade or clades to be rare, and have so far found 1/121 Omanis, 2/150 Iranians, 1/164 in the United Arab Emirates, 3/612 in Turkey. Mutations understood to be equivalent to M420 include M449, M511, M513, L62, L63.^[2][3]

Correcting that section First, if it helps break it up into sections as follows

Recently, the labels associated with different branches of the R1a family tree (phylogenetic tree) has been updated. This has resulted in a shift in the names (nomenclature) applied to the branches R1a, R1a1, and R1a1a.

Hey I haven't been on for a while and got your message on my page. Just wanted to thank you and show my appreciation. I've been sitting back watching the page and it's seems Andrew has hijacked the page and is obsessively paranoid. I will start contributing to the article to show my balance and support. I think it's time we balanced the article by expanding the South Asian Origins section and removing alot of the cherry picked, inconsistent, old data being presented as a sealed deal. I'm willing to work with everyone, but they seems hellish on the Linguistic theories...which is 3-4 times the size of the South Asian section. I wrote a big thing on the R1a talk page. Let me know - Thanks!! HonestopL 15:08, 18 January 2010 (UTC)

Hi, I have contributed to the discussion about the page [] and I have not seen any replies or concensus about what to do. I'd apprecite your comment, your views on how to improve those pages. I am willing to do some work. Cheers, rené Renebach (talk) 21:09, 27 January 2010 (UTC)

I have finished a first pass at cleaning up the Haplogroup R1a (Y-DNA) page, which you were also editing until a short while ago. It's still somewhat rough about the edges, and has a pending proposal to split off the origins hypotheses stuff (because that's all speculation and an inevitable magnet for cruft and POV-pushing, so we might as well localize that ongoing edit-war), but in essential outline I think the page is now functionally and logically complete. What do you think? For reference, this is the version I'm talking about. And you may find this thread interesting. rudra (talk) 05:38, 19 February 2010 (UTC)

I have once again removed erroneous information and a photo (not related to the vessels) with an inaccurate caption concerning the aforementioned vessels that were affected by the September 1, 2008 surge in the New Orleans Inner Harbor. I have removed reference links to articles in the Times Picayune newspaper that contained inaccurate information, including inaccurate information about Southern Scrap and the Army Corps of Engineers and what happened during Hurricane Katrina.

The Courier, American Explorer, and Hunley were wrested from their moorings by the Hurricane Gustav surge on the morning of September 1, 2008. There was no damage to any bridges or structures by the Courier, American Explorer or Hunley and, working with the USCG, the company successfully re-moored the vessels and dismantling was continued. —Preceding unsigned comment added by Visavixen (talk • contribs) 15:26, 2 March 2010 (UTC)

Hello, Pdeitiker.

Maybe you will be interested in this issue. In Brazilians of Spanish descent, this paper, by Brazilian geneticist Andrea Rita Marrero, is used as a source for the information that "Gaúchos [...] are mostly descended from Spanish ancestors, and less from Portuguese". As this runs contrary to mainstream knowledge about the region, it would be interesting to understand what exactly are the bases for the paper's conclusions. Another paper by the same scientist (in collaboration with others) gives more details about the subject. Could you please help us with this subject?

Thanks in advance. Ninguém (talk) 12:49, 13 July 2010 (UTC)

There is a discussion about some content you created here. You are welcome to join if you wish. Biophys (talk) 18:54, 27 July 2010 (UTC)

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I hope this will enhance your editing, and allow you to edit successfully and without disruption. - Alison ^❤ 12:11, 25 March 2011 (UTC)

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Talk:Air_France_Flight_447#In-depth_information_regarding_latest_report

• Need for intergration of all available data has been expressed and your ACARS table could be a start; need help.

Patelurology2 (talk) 21:29, 2 June 2011 (UTC)

Please review and comment:
http://en.wikipedia.org/wiki/Haplogroup_J1_(Y-DNA)
http://en.wikipedia.org/wiki/Talk:Haplogroup_J1_(Y-DNA)
JohnLloydScharf (talk) 00:10, 22 August 2011 (UTC)
Thank you for your timely and detailed response. I was surprised, as you seem to be, at the departure from research methodology by using anything less than n=30 for a sample population. Saying a nation is a certain way by sampling students tells me about students rather than the nation, whether it is politics or genetics. I think you need 2000 samples, but at least 600 would be good and 12 will not do. However, what do I know.... I only took three research classes at the 400 level; one for psychology, one for sociology, and one for math classes, but that experience changed my perspectives and expectations about probability and statistics. Even political polls are off with less than 1600. JohnLloydScharf (talk) 23:48, 22 August 2011 (UTC)

http://en.wikipedia.org/wiki/HLA-DQ1#Gluten-sensitive_neuropathy_controversy
Do you know what OTHER three SNPs are associated with this?

Effective Detection of Human Leukocyte Antigen Risk Alleles in Celiac Disease Using Tag Single Nucleotide Polymorphisms http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2386975/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685746/ http://www.ncbi.nlm.nih.gov/pubmed/18509540 http://www.snpedia.com/index.php/Gs221

This genoset tags the DQ2.2 haplotype in Europeans, and thus increased risk gluten intolerance and for autoimmune disorders such as celiac disease.[PMID 18509540] http://www.snpedia.com/index.php/Gs221/criteria

I am not able to interpret the above, have data on my own personal SNPs of the three in that reference.

• rs2395182 chromosome 6 nt position 32521295 TG - DQ2.2, DQ4
• rs7775228 chromosome 6 nt position 32766057 TT - DQ2.2, DQ4
• rs4713586 chromosome 6 nt position 32767560 AA - DQ4

John Lloyd Scharf

" At first the sensitivity and specificity for DQ2.2 was high and accurate but the predictive value was low. The SNPs for DQ2.2 (rs2395182, rs7775228) not only tagged DQ2.2 but also included the relatively infrequent DQ4 allele. We therefore decided to tag DQ4 as well (rs4713586) making it possible to call a person DQ2.2 when the alleles were positive for DQ2.2 and negative for DQ4. This led to three tag SNPs being needed for the prediction of DQ2.2, with an overall sensitivity of 0.992, a specificity of 0.998 and a PPV of 0.977. Only four of the 1448 tested chromosomes gave false results (0.28%). "

DQ2.5cis haplotype is tagged by: "The tag SNP selected for prediction of DQ2.5 (rs2187668) showed an overall sensitivity of 1.000, a specificity of 0.999 and a PPV of 0.998. Only one of the 1458 tested chromosomes gave false results (0.07%). This person did indeed carry half of the DQ2.5 haplotype (DQA1*0501)"

And in fact the haplotype DQA1*0501 DQB1*0202 exists in Africa along with *0505 - *0202. There are also evidence of some Linkage Disequilbrium in Norway.

DQ2.5 cis haplotype is tagged by DQ2.2 tags and: "The tag SNP for DQ7 (rs4639334) showed an overall sensitivity of 1.000, a specificity of 0.997 and a PPV of 0.959. Four of the 1470 tested chromosomes gave false results (0.27%), of which three carried a rare haplotype consisting of half of the DQ7 haplotype. Two of these three carried a combination of the DQA1*0505 allele of DQ7 with the DQB1*0302 of DQ8 (see results of DQ8 as well) and were predicted to be both DQ7 and DQ8 (see Table S3b, person nos. 11 and 12). For one of these persons we typed the parents and we could see a transmission of this combined haplotype in the family."

DQ8.1 haplotype is tagged by: "The tag SNP for DQ8 (rs7454108) showed an overall sensitivity of 0.991, a specificity of 0.996 and a PPV of 0.948. Seven of the 1484 tested chromosomes gave false results (0.5%)."

This captures, according to the European study 99.97% of all celiac cases.

The danger of using DQA1* tags for celiac disease is that DQB1* confers most of the risk, and risk remains when DQA1*0501 or *0505 are absent. Consequently one has to use both DQA1* and DQB1* tags to accurately detect DQ2.5cis bearing haplotypes. If you are typing patients in Western Ireland, you are going to get the haplotype right no matter what, but if you are typing in N. or W. Africa, particularly in Cameroon, there is a good chance you will tag it wrong.

If fact, during our recent MG study in Houston we found the following haplotype DQA1*0401:DQB1*0201 (an as yet identified haplotype).

Regarding the GSIN. They claim and have never done high resolution studies that I know of, i have presented their findings but disagree with their conclusions. The associated serotype is DQ1. DQ1 is subdivided into DQ5 and DQ6 based on beta chain immunoreactivity. This represents a dozen haplotypes and multiple variants. PB666 ^yap 22:02, 23 August 2011 (UTC)

• Okay, I just discovered you responded. See if I interpret this correctly. Your examination and interpretation of my SNPs is I am DQ4, which is not associated with Celiac or gluten intolerance. That is consistent with my not having a diagnosis of having those. I had a "Family Finder" test done by FTDNA. I have a file for a batch of autosomal SNPs and X SNPs. I have had over 120 yDNA STRs and a full sequence of my mtDNA done by them as well. I want to learn how to read/understand these SNPs and Chromosome 6 is as good a place to start as any.

• My interest was initially in genealogy for testing, but I have always had an interest in archaeology since my pre-teen years. That is why I am interested in ancient DNA and how haplogroups line up with such things as Pre-Pottery Neolithic. The more I look at how they structured yDNA haplogroups, the more I am reminded of how they base everything in mtDNA, as well as some of HLA, is based on a woman who died the year I was born. At least HLA has a practical use, like ABO.

Thanks for the additional information on my talk. I have had something in the back of my mind for quite some time. How do they determine what an "ancestral" allele or SNP by just molecular rather than historic means? John Lloyd Scharf 18:35, 24 August 2011 (UTC) Also, I posted a response to your message on my talk page. John Lloyd Scharf 20:16, 24 August 2011 (UTC)

Maps are hard, you have to both follow wikis, often silly, rules (And they are, for instance if two papers give to ranges for dates say 85 to 135, and 125 to 235, both studies cannot be correct, but you cant then say the date range is 85 to 235, that is a synthesis, even though the wiki admins cannnot decide which is best or correct to give in the article, IOW they force a concensus to cherry pick rather than actually represent scientific range) and avoid the legal issues. At the same time you can't assume one author did correct research in reading others M and M section of papers included in his graph, so you have to actually read papers and see where these study points represent.

It is the Abilene paradox demonstrated by Wikipedia consensus decision-making. If the ultimate objective is not to "rock the boat", then reality is defined the effort to appease everyone while informing no one. John Lloyd Scharf 23:44, 23 August 2011 (UTC)

• "rs2421826","11","35187181","GG"

http://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?rs=rs2421826

This allele is not listed and it is the result I got from Family Finder DNA. Is it possible there has been a malfunction,

http://www.ncbi.nlm.nih.gov/pubmed/19877174

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020103/

John Lloyd Scharf 04:02, 9 September 2011 (UTC)

ref_assembly - 35187181 G

GG is a phenotype, it means that a state (i.e. individual, risk phenotype, or etc:something representing both strands of chromosome 11) and that both sister chromosomes are in the same state.

The mutation appears not to be part of a CNV

"In fact, half of the reported SNPs are still only candidate SNPs and are not validated in a population. We describe the identification of SNDs (single nucleotide differences) in humans, that may contaminate the dbSNP database. These SNDs, reported as real SNPs in the database, do not exist as such, but are merely artifacts due to the presence of a paralogue (highly similar duplicated) sequence in the genome."

There are several things one has to remember about SNPs.

• Many SNPs are restricted to closely related lineages and are excluded from the population after a few generations, mostly by drift, sometimes by negative selection.
• SNPs in the databases are usually quite common in some populations and are well characterized. Most (if not all) of the SNPs that you and I will ever deal with are sufficiently characterized . . .But:

-The order of the SNPs on different peoples chromosomes may not be characterized, in general the order of SNPs on the chromosome is assumed however I know researchers that have questioned both the order of SNPs and the direction on the chromosome.

-Some SNPs are part of larger variable units (indels) and these insertions are often variable in size.

-Some SNPs that have been characterized have been characterized cells of clonal origin that represent mutations that are not carried in the germ-line DNA. Sometimes the mutations are a found frequently. I can give examples where a somatic mutation is commonly found in cells with cancer, the non-cancerous cells dont carry the mutation, but the cancerous cells often do.

PB666 ^yap 21:47, 13 September 2011 (UTC)

• When you say "restricted to closely related lineages," I think of the so-called CEU population used to represent Europeans. Every time I look at an individual in that group, they are clearly stated to be "Morman." (Example: http://www.ncbi.nlm.nih.gov/SNP/snp_ind.cgi?ind_id=171 )

By the way, when they claim "Caucasian/UTAH/MORMON" I know there is an ignorant bias. It sends up a red flag when they use "Caucasian" and may as well be "Aryan." Unless their genetic/geographic origin from between the Black Sea and Caspian Sea, they are just another Western European type. The British Isles are distinctly different than even mainland Western Europe. I think we need a group other than Northeast Utah LDS to represent "Europeans." John Lloyd Scharf 17:54, 14 September 2011 (UTC)

The CEU sample for the USA comes from the Mormon population of Utah.PB666 ^yap 19:45, 14 September 2011 (UTC)

There is not one genetic background for England. Ireland, Scotland, NW England, Wales can be distinquished from the rest of England by the unusually high level of ancestral haplotypes. The Cornish population is this plus some other (presumbably phonecian) influences. Central England is cosmopolitan, but the core Ethnic Anglo group shows relatively high presence of Latin (French, Italian, Spanish) influences whereas SE England tends to reflect the genetic makeup on the other side of the Channel (Netherlands, Belgium, N France, N. Denmark).

By and large, the genetic makeup of Americans tends to most closely reflect people of NW Ilse region and Scandinavia with a slight tilt toward German. British proper are not very representative of Europe as a whole, I suppose the french are probably the most representative, but there has to be a cost paid because if you are trying to distinguish European descent (e.g. North of the Italian Alps, West of the Carpathian Mts) from Middle Easterners and Meditteraneans, France and Belgium have particularly high levels of fingerprint HLA from NE Mediterranean, Eastern Black Sea region, and the Levant. France is an antinode within the standard repertoire HLA haplotype nodes (A1-B8-DR3-DQ2.5, A3-B7-DR15-DQ6.2, A2-B7-DR15-DQ6.2, and A2-Cw5-B44 haplotypes). That does not help much if you are trying to distinquish a European enriched disease from disease of other parts of the world.

IMO at this stage of the game, with 100 European HapMapped one does not expect a high level of precision. I would be more concerned about founder effects in the Mormon population, but this can be diluted with selected sampling from good geneologies, which they have. There, of course, is no way to do Y-VNTR of long deceased males to confirm paternity, and when monogamy in Utah's rural area is a joke, then we can basically argue that paternity can be called into question. Such patterns of concealment of paternity can lead to unseen rapid drift. Nonetheless the level of precision for the designator CEU, given the rather undefinable nature of the designator is adequate. Once we get 10,000s of European Genomes types by SNP, then it should be possible to look at say Western Irish, Southern Irish, Northern Irish and Eastern Irish. This will reveal SNPs that evolved locally and expanded over prehistoric time, but with a low level of backflow their presence in Europe would be treated as rare to 'nascent mutation'.

Consider other sources of error:

-Faulty assay materials (this was observed and published upon recently, a researcher got a batch of plates that gave unusual results, after testing the plates he found they were not reporting as per manf.

-Mistyped SNPs and somatic mutations.

PB666 ^yap 19:45, 14 September 2011 (UTC)
Because of the famine caused in Ireland by the British and in stealing lands from the Scots, the influx of immigrants from those regions in the beginning in the late 1700s to the late 1800s the genetic make-up of the US is decidedly Scots-Irish. The LDS founders who produced the most offspring are from Anglia where Scandinavian Influence is stronger from prior to 1000 AD. I believe seven generations washes out most alleles, but there is little left after 16 and more. Being an island nation brings a lot of isolation. The is aggravated by a couple dozen founders, some of which were already related, having up to 50 offspring. The deeper the roots in LDS, the higher the probability of red hair and dark eyes.
I doubt we shall see 10,000 Irish genomes anytime soon and there is little standardization in how the haplotypes are being read. At this point, this "science" looks more like astrology than astronomy and the "genetic genealogists" are quick to muddle the interpretations for the results, if not the researchers themselves. They declare no biases, but there is more than financial interests involved. John Lloyd Scharf 02:58, 17 September 2011 (UTC)

• I have been looking at a section of my Chromosome 2 because I match that section with someone else. This mentions A, AA, AG, G, and GG genotypes. I have been tested and the genotype stated is CC. Should that be interpreted as a GG?

Illumina-"rs884460","2","140642488","CC"

Affy-rs884460 2 140642488 CC

http://www.ncbi.nlm.nih.gov/projects/SNP/snp_ref.cgi?rs=rs884460

John Lloyd Scharf 19:19, 10 October 2011 (UTC)

Yeah, that is one of the screwiest looking SNPs I've seen. The sense strand to me looks like T, not A, and therefore what they you CC is right. Why on the page they you A/G versus T/C is simply confusing the issue.PB666 ^yap 21:18, 10 October 2011 (UTC)

Okay, so it is not some magical mystery I just am ignorant of. I ran into "one of those" like the one you have problems with here on SNPedia. He is just a software type. There are many like this listed there. I can see why you recommended NCBI. They are muddy, but this guy just aggravates that. Much of the research seems not to be relevant to my medical issues and the risk alleles are not named more often than not. Today I found SNP listed on SNPedia claiming to be for a Haplogroup on Y and it was listed as Chromosome 2 and actually referred to a SNP for Chromosome 5. It is like Wikipedia in that it is edited with incompetence by Gene Nazis. ;>John Lloyd Scharf 02:49, 11 October 2011 (UTC)

Chromosomal position number more or less arbitrarily choose one 5' to 3' direction off of one end of the chromosome. The sequence that they obtain is from contigs that oriented from the other end. Its easy to 'transform' the contiq sequence to make it a + strand and avoid the confusion. The problem here is that in some cases substitutions are not transitions, but transversions, and the - strand contigs have the same sequence as the minor variant. It gets confusing and you have to dot your i's and cross your t's when working with this stuff. Moreover some SNPs are actually part of insertions and deletions, which means the adjacent variants are not included. Its a headache. Try processing 1000s of these SNPs as I was doing earlier this year. I actually had a macro in microsoft excel VB application that would search out the SNP page for adjacent variants downloaded from the hapmap, and was able to deduce the major and minor variants. I can say that most of the SNPs presented from genome wide association studies are not causal mutations, they are linked to causal mutations. The GWAS do not present a fair representation of linkage disequilibrium or the representation density of haplotype variants already described by HapMap. As a consequence an SNP linked to any given low penetrance causal variant could be a million nucleotides from that causal variant. It was not uncommon to see GWAS associations that were later to be shown as QTL loci 50,000 to 500,000 nucleotides away from the GWAS SNP associated. GWAS are great, BUT they generally do not disclose their weaknesses.PB666 ^yap 21:48, 14 October 2011 (UTC)

1. That they are representative, only about 1 per 100 known SNPs in any given population are used. 2. That they are corrected, and without a highly refined assessment of linkage disequilibrium between representative markers, the correction method is likely to underestimate probability. 3. That because they are representative, regional associations are generally not maximally optimized. 4. That because of 1 - 3 that many associations are missed, marginal associations that exist between the broad band between uncorrected and corrected probability thresholds.

Medical issues are difficult to deduce with random genetics. SNPs, unfortunately generally do not equal genes (as in functional allelic variants at disease-related loci).PB666 ^yap 21:48, 14 October 2011 (UTC)
As a teen I was a pheasant hunter. I had some old ammo. When I pointed directly at a rooster flying away from me dirt flew up all around the bird, but it had no reaction. It fired a lead donut of bird shot. Chromosomes and mitochondria are not all the same in their order for each individual, if my mtDNA is any example. I have no deletions, but I do have extra basepairs at certain points than the Cambridge model. I think the problem, from what you are saying, is that a SNP may or may not affect the function of a gene. I always wonder if that old term "junk DNA," may be a load of redundant genes that either correct what a malfunction does or actually acts as a backup to do that function of the gene. However, I do continue with my personal DNA testing with the hope that it will be useful to my offspring, if not myself. I have hypertriglyceride levels and Type II Diabetes [insulin resistance]. I think the two are connected and I may be thyroid "resistant" as well. John Lloyd Scharf 05:31, 15 October 2011 (UTC)

CRS sequence is not stable, it has changed several times since it was first sequenced. It is known that if you take sequence from different body tissues for CRS bearing individuals you will get different sequence. There are several points in the HVR2 region that account for this instability.

We are not asking the question about Junk, although it is a valid question with many SNPs. The question that the association begs is whether the SNP is involved (either causal or protective) in disease or is simply a representative marker, or in some cases random marker. Since there are a large many diseases that have inherited components, then there is a possibility that some of the SNPs associated with certain disease are causal with other diseases (unlikely but plausible in most instances). This is the way statistics works sometimes. We have to ask simple binary questions, then correct later on with the issue of multiple sampling or analysis.

[Most of post refactored, see history]PB666 ^yap 20:10, 24 October 2011 (UTC)

My point in saying this is that certain foods may not be recommended to the general public, but for some people, those foods may be the best source of protein and fat, and common foods like beef, wheat-containing foods, high starch diet are 'more or less' poisonous. PB666 ^yap 07:09, 15 October 2011 (UTC)

This seems to be what my specialist is telling me. John Lloyd Scharf 23:20, 21 October 2011 (UTC)

Hi, I'm translating Anti-mitochondrial_antibody into Chinese. There is one thing I'm not quite sure about because I'm not professional in this field. Would you please tell me that the relationship between

• pyruvate dehydrogenase, E2 subunits
• 2-oxo-glutarate dehydrogenase
• branched chain 2-oxo-acid dehydrogenase

and

• AMA
• PBC

Do you mean that "pyruvate dehydrogenase, E2 subunits", 2-oxo-glutarate dehydrogenase and branched chain 2-oxo-acid dehydrogenase are the "major liver antigens"?

Thank you. Sumtec (talk) 06:36, 27 October 2011 (UTC)

Primary biliary cirrhosis (PBC) is a type of autoimmune liver disease.

The disease is caused by the progressive obstruction of the ductile facilities of the liver resulting in the backup of bile into the liver. Complete obstruction causes endstage liver disease.

Antibodies in PBC react with the ductile cells. There are two major catagories.

1. Reactivity to Nuclear proteins. (e.g. Anti-gp210 antibodies). Reactivity to the nuclear proteins is the best evidence for progressive (toward endstage disease)
2. Reactivity toward anti-mitochondrial antibodies (AMA). The importance of their involvement is not so clear.

While using the "word major liver antigens" could be used, it is probably not appropriate. First, these are not the antigens that typify the most dangerous form of disease, second these cells are liver cells but that are specialized components of the ductile tissue that drain the liver (as opposed to venous tissue or hepatocytes). They are the most common antigen of these tissues. There is autoimmune liver disease that attacks hepatocytes, so . . . . .

http://www.cpmc.org/advanced/liver/patients/topics/hep_autoimmune.html

AMA are, at least, indicators of the occurrence of a destructive anti-ductile tissue immune response. Not sure that they are pathological autoimmune targets. This page is somewhat obsolete and you might try looking up more recent papers on AMA involvement in PBC on Pubmed.PB666 ^yap 16:21, 27 October 2011 (UTC)

The Y chromosome is abstractly described as a highly differentiated variant of the X chromosome. This definition might be considered an oversimplification of the reality because all chromosomes are "highly differentiated variants" of other chromosomes. But in the case of the Y chromosome the analogy has more specific meaning.

1. There is a region of the Y chromosome which is called NRY (non-recombinant portion of Y). This makes up the majority of the y chromosome.

2. The remainder is the recombinant portion of Y which has analogous sites on the X chromosome. The SNPs on Y that are close to recombination hotspots have comparable sites on X. These sites are spread widely across the x chromosome but are packed into a small region of Y.

3. The basic concept of recombination is that you have similar regions on two chromosomes in which the recombination machinary can build a "X" structure that then can resolve itself. Therefore the fact that X and Y can undergo recombination means that there are sites between 20 and 100 nts in length that are nearly identical between X and Y. Statistically we have to think about this. If there are 4 nts used at roughly the same frequency the odds of a match is 1/4 for 1 nucleotide, 1/16 for 2 nucleotides, 1/64 for 3 nucleotides. By the time you get to 17 nucleotides in length the probability of exact match of 2 sequences is less than 50% for the entire genome. Therefore for specific recombination to work the matching needs to be for sequences >16 nts in length. (Otherwise Y would recombine with other chromosomes or other parts of X). To get it down to the point that no recombination site will undergo false recombination you need recognition of approximately 25nts. What Parhan and Ohta found in 1986 is that to achieve gene conversion in the HLA class I, typically lengths of 30nt were resulting in abortive recombination if there was a single or multiple mismatches. So somewhere between 22 residues and 1 mismatch (favoring gene conversion) and 30 nts with no mismatches favors (classic recombination). BTW, if gene conversion occurred between 2 improperly paired but similar sequence, we would not identify these as convertants, they would appear to us as point mutations as a result of some other cause.

4. There are other areas of Y scattered widely and at very low density in the Y chromosome that have undergone some 'recombinative' activity with X, probably some form of abortive recombination. This indicates that an adequate amount of sequence conservation has persisted in parts of the NRY.

5. The NRY of Y evolves in a anomalous manner relative to other chromosomes. Comparison of chimpanzee and human Y chromosome has revealed that vast regions of Y have undergone marked insertion and deletion events. The so-called STRs have a tendancy to expand and contract greatly as new STRs appears and old STRs disappear. Interdispersed in these are stretches of somewhat conserved DNA that mutate at an elevated but autosomal like rate. Our understanding of how Y chromosome evolves is far from complete. I expect that in the next few years as many human Y are fully sequenced and we get more information from the Y chromosomes of archaic homo sapiens aDNA sequence, as well as multiple chimpanzee and gorilla Y chromosomes, we will have a much better picture of how the Y chromosome is evolving. Lets just say right now that there is evidence of spurts of evolution in Y chromosome in anthropoid apes.

To solve your question, you have to do a little homework. Match the positions of the sequence in the X chromosome with those found on the Y. To do this use the sequences of the variants and do seaches. You might be able to reconstruct in your head a diagram of comparative structure of X and Y.PB666 ^yap 17:00, 28 October 2011 (UTC)

Monotrenes, such as platypus have bird like Y chromosomes, this indicates that our version of Y started evolving around 150-250 million years ago, after birds (dinosaurs) and mammals (from therapsids) split.

http://en.wikipedia.org/wiki/Y-chromosome

Genome Res. 2008 Jun;18(6):965-73. Epub 2008 May 7.Bird-like sex chromosomes of platypus imply recent origin of mammal sex chromosomes.Veyrunes F, Waters PD, Miethke P, Rens W, McMillan D, Alsop AE, Grützner F, Deakin JE, Whittington CM, Schatzkamer K, Kremitzki CL, Graves T, Ferguson-Smith MA, Warren W, Marshall Graves JA.

"In therian mammals (placentals and marsupials), sex is determined by an XX female: XY male system, in which a gene (SRY) on the Y affects male determination. There is no equivalent in other amniotes, although some taxa (notably birds and snakes) have differentiated sex chromosomes. Birds have a ZW female: ZZ male system with no homology with mammal sex chromosomes, in which dosage of a Z-borne gene (possibly DMRT1) affects male determination. As the most basal mammal group, the egg-laying monotremes are ideal for determining how the therian XY system evolved. The platypus has an extraordinary sex chromosome complex, in which five X and five Y chromosomes pair in a translocation chain of alternating X and Y chromosomes. We used physical mapping to identify genes on the pairing regions between adjacent X and Y chromosomes. Most significantly, comparative mapping shows that, contrary to earlier reports, there is no homology between the platypus and therian X chromosomes. Orthologs of genes in the conserved region of the human X (including SOX3, the gene from which SRY evolved) all map to platypus chromosome 6, which therefore represents the ancestral autosome from which the therian X and pair derived. Rather, the platypus X chromosomes have substantial homology with the bird Z chromosome (including DMRT1) and to segments syntenic with this region in the human genome. Thus, platypus sex chromosomes have strong homology with bird, but not to therian sex chromosomes, implying that the therian X and Y chromosomes (and the SRY gene) evolved from an autosomal pair after the divergence of monotremes only 166 million years ago. Therefore, the therian X and Y are more than 145 million years younger than previously thought."

Therefore it appears that mammals evolved a male heterogamy system from a female heterogamy system. There is a review that discusses this "Sex-chromosome evolution: recent progress and the influence of male and female heterogamety", Hans Ellegren Nature Reviews: Genetics 12:157, where they outline the evolution. The monotreme chromosome 6 (m6) is the male-quiescent arm of chromosome primates (XY). PB666 ^yap 19:55, 31 October 2011 (UTC)

Thanks for pointing out the above information. It was far afield from what I was looking for, but interesting to me and useful to the head of the science department of a high school who I share with regularly. As usual, I get a broader perspective from you than my original intent, which I am thankful for. John Lloyd Scharf 21:20, 31 October 2011 (UTC)

J is a subclade of IJK, which is a subclade of F. Here is a conundrum for you. If J is a subclade of F, does it have all the SNPs of an F? Is it possible for someone only tested for F SNPs to be a crypto - J1? John Lloyd Scharf 22:20, 31 October 2011 (UTC)

There is always a risk of a reverse mutation, but reverse mutation of single site polymorphisms on Y are incredibly rare. I would say that not enough markers were typed in that example. Frequently in HLA analysis one strategy was to define the group markers first, after defining the group markers select from a shorter list of subgroup markers and then get a refined analysis. HLA analysis is so far ahead of Y that now we can define the overwhelming majority of human major antigen HLA at the refined level in a single step.PB666 ^yap 15:59, 1 November 2011 (UTC)

I am not referring to a reverse mutation. J1 is a subclade of F. You have to qualify to be an F in order to be a J. F>IJK>IJ>J>J1 is the progression from clades to subclades. I am trying to see if the testing assumptions excluded testing for J just because an F SNP was found.

Check these results of mine:

• Haplogroup J1

rs9341313 Y 21151206 G [Indicates a J1 subclade]

• Haplogroup I

i4000186 Y 12994387 C [Indicates an I subclade]

Regarding HLA, I have been thinking about it as a way of establishing ethnic roots for a couple years now and the information in that area has exploded since I first became conscious of it. The Y chromosome is only 70,000 years old. HLA for homo sapiens sapiens began developing before the existence of mitochondrial Eve 200,000 years ago, if not for the past 535 million years. It is a unique survival strategy for a small group where some HLAs survived over others as humans existed in small families and tribes over 5200 years ago. If HLA testing of surviving dental pulp was done from remains, it would go a long ways toward advancing cultural anthropology. Establishing Y chromosome origins will likely come from HLA research.

John Lloyd Scharf 16:23, 7 November 2011 (UTC)

Hello there,

You've put in much dedicated work and are far ahead of me in your Wikipedia savvy, but I want to do what I can to contribute to the Y-haplogroup A page, as I have been intensively (as best I can with a full-time job) studying this clade for much of the past year, and am now helping to coordinate research on it. I have just finally posted the 2012 ISOGG phylogenetic tree for Haplogroup A, and the Wikipedia page needs to be updated to reflect it. I wonder if you can help with this task.

I understand that you are sensitive to the requirement that original research not appear in Wikipedia articles, but once we at ISOGG analyze the new research findings and incorporate them into our tree, which is then published on our website, my impression is that it has been considered a valid source for Wikipedia.

I just stopped by the Haplogroup A article and noticed a small error, that the Yorkshire members of A were entered under A2-T, when in fact they are A1a-M31, as it states in King's original article. I added that material to the A1a section.

Even updating the phylogeny to the ISOGG tree that we have today, won't be a fix for very long, as dozens of new SNPs are being discovered through Walk Through the Y sequencing, which are adding and modifying branches.

So, there is much more that needs to be done -- I don't know the best place to start. Suggestions for what I can do that would be most helpful with the least input of very limited time? Iris-J2 (talk) 19:59, 18 February 2012 (UTC)

06~03~2012~15.32~

Hello, if possible, would you please be so kind to give me the corrisponding meaning of certain genetic markers? I'm searching the internet and having problems, the appointment with the doctor is still far and I'm eager to find out what they mean, thank you in advance for any help.

My 3 y.o. son was tested as follow:

HLA A 01, 11 HLA B 51, 57 HLA C 06, 15 HLA DRB1 07, 14 HLA DQB1 03, 05

DR14-DQ5 = DRB1*1401 - DQA1*0104 - DQB1 *0503 is a DR-DQ (e.g DR14 DQ5) haplotype it is sometimes associated with very rare instances of MuSK antibody positive myasthenia gravis. The risk is very very small DR7-DQ3 = DRB1*0701 DQA1*0201 DQB1*0303 most of the time. This haplotype is not overly common but it is of increased frequency in areas of Europe and Asia with recent African contribution. DQB1*0303 also called DQ9 is associated with a few AID. The HLA mediated risk for type 1 diabetes and celiac disease are neglegible. For Rheumatoid arthritis ther is some unknown level of risk for the 05 locus (*0501 associates with RA, but not known for DQA1*0104 : DQB1*0503)

A*01 Cw*06 B*57 is a haplotype found in western Europe. It is the core component of the A1-B57-Cw6-DR7-DQ9 haplotype. It is my suspicion that this haplotype, specifically, is associated with psoriatic arthritis (PsA). To be clear, this is a very long range haplotype in a region that may contain over 300 genes. We do not know which of these genes causes psoriatic arthritis but we do know that that Cw6 (HLA C 06) is the best marking allele and is elevated in PsA. This haplotype in Poles, Irish, Spanish is likely due to a recent identity-by-common-descent from a single ancestor, probably not more than 10,000 years ago.

Balding J, Kane D, Livingstone W, Mynett-Johnson L, Bresnihan B, Smith O, FitzGerald O. Cytokine gene polymorphisms: association with psoriatic arthritis susceptibility and severity. Arthritis Rheum. 2003;48:1408-1413. González S, Martínez-Borra J, López-Vázquez A, García-Fernández S, Torre-Alonso JC, López-Larrea C. MICA rather than MICB, TNFA, or HLA-DRB1 is associated with susceptibility to psoriatic arthritis. J Rheumatol. 2002;29:973-978. Grubic Z, Peric P, Eeèuk-Jelicic E, Zunec R, Stingl K, Curkovic B, Kerhin-Brkljacic V. The MICA-A4 triplet repeats polymorphism in the transmembrane region confers additional risk for development of psoriatic arthritis in the Croatian population. Eur J Immunogenet. 2004;31:93-98. Ho PY, Barton A, Worthington J, Plant D, Griffiths CE, Young HS, Bradburn P, Thomson W, Silman AJ, Bruce IN. Investigating the role of the HLA-Cw*06 and HLA-DRB1 genes in susceptibility to psoriatic arthritis: comparison with psoriasis and undifferentiated inflammatory arthritis. Ann Rheum Dis. 2008;67:677-682. Deitiker PR, Oshima M, Jankovic J, Duane DD, Aoki KR, Atassi MZ. Association of HLA Class II alleles and haplotypes with cervical dystonia: HLA DR13-DQ6 (DQB1*0604) homozygotes are at greatly increased risk of cervical dystonia in Caucasian Americans. Autoimmunity. 2011;44:167-76.

If my deduction is correct then it means that the other haplotype is: A11 Cw15 B51 DR14 DQ5 (HLA A 11, B 51, C 15 . . . ). Parham believes that A11 evolved from a Neanderthal-like humans (Desanovans/Narmadans) that once lived in eastern Asia (In other words it is not from Africa as recently as %96 of most human genes). The Cw15 B51 is found more commonly in Asia and Middle eastern regions. DR14-DQ5 also spreads across northern Eurasia. The A11 allele may be protective for Asian water borne diseases. The only noted full length haplotype has been found: A*11:02-B*51:02-C*15:02-DRB1*14:01-DQB1*05:02 was an Asian American, noting that when the study was done DQB1 may have been mis-subtyped and the frequency is very low. The frequency mode for A11 Cw15 B51 is between Poland and England. C15-B51-DR14 is found considerable more frequently in Asians than Europeans (mostly poles). The DR14-DQ5 segment is modal in the China Yunnan Province Drung, more than likely this part of the haplotype originated in the surrounding regions of Asia.

In terms of risk associated with this. It is generally at such a low frequency risk is not commonly associated. Risk was found with Muscle Specific Kinase antibody (anti-MuSK) autoimmune myasthenia gravis, and our work here in Houston supports that assertion.

Int J Immunogenet. 2011 Feb;38(1):55-62. doi: 10.1111/j.1744-313X.2010.00979.x. Epub 2010 Nov 25. Association with HLA DQ of early onset myasthenia gravis in Southeast Texas region of the United States. Deitiker PR, Oshima M, Smith RG, Mosier D, Atassi MZ. Strong association of MuSK antibody-positive myasthenia gravis and HLA-DR14-DQ5. Niks EH, Kuks JB, Roep BO, Haasnoot GW, Verduijn W, Ballieux BE, De Baets MH, Vincent A, Verschuuren JJ. Neurology. 2006 Jun 13;66(11):1772-4.

Again the risk is very rare, something like 1 in a million have this form of myasthenia gravis. Even amoung people who have DR14-DQ5 the risk is 1 per 100,000 or so. PB666 ^yap 23:54, 6 March 2012 (UTC)

p.s. you can email me at pinklunamoon@hotmail.com thank you

— Preceding unsigned comment added by 87.20.185.184 (talk) 14:36, 6 March 2012 (UTC)

Hi, I just came across User:Pdeitiker/Soil Moisture and Ocean Salinity (SMOS) satellite and replaced it with a link to the live article.

Please would you have a look through Special:Prefixindex/User:Pdeitiker and tag any user sub-pages with {{db-author}} if you do not need them any more? WP:STALEDRAFT explains why.

Also, this talk page is rather long. If you would like to archive it, see WP:ARCHIVE for alternative methods, or I'd be happy to do it for you; please drop me a note if I fail to respond here. Best wishes, – Fayenatic London 18:35, 19 December 2012 (UTC)

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