For Salty

To easy salty...it is hardly a case of semi-meiosis...these tumors are called dermoid tumors and are not semi-meiotic but typcial cancerous abnormalitiesCancer Genet Cytogenet 2001 Feb;125(1):59-62 Related Articles, LinksChromosome analysis and comparison of the benign cystic and malignant squamous component of an ovarian teratoma.Noumoff JS, LiVolsi VA, Deger RB, Montone KT, Faruqi SA.Crozer-Chester Medical Center, Upland, PA, USA.Teratoma, the most common ovarian germ-cell tumor, presumably arises from a single germ cell and is composed of tissues representing all germ layers (ectoderm, mesoderm, and endoderm). Benign cystic teratomas (dermoid cyst) represent over 95% of ovarian teratomas and are comprised of entirely mature adult tissues. When malignant, almost all mature teratomas contain squamous carcinoma. We report for the first time the karyotypic comparison of an ovarian teratoma in a 36-year-old female with tissue separately taken from the benign cystic and malignant squamous components. The malignant squamous component revealed two distinct karyotypic populations: one diploid and the other polyploid. Both, however, demonstrated two common markers. The polyploid population also demonstrated numerous additional abnormalities with multiple copies of chromosome 20. Though many of the chromosomal aberrations were unique to the benign component, several karyotypes showed the same markers noted in the malignant squamous component. The significance of this finding is that it may serve to identify those histologically benign teratomas destined to undergo malignant transformation.And the so called miraculous appearance of teeth and hair in these tumor types is merely a reflection of the undifferentiated state of germ cells and their pluripotentialityCancer Res 2003 May 1;63(9):2244-50 Related Articles, LinksPOU5F1 (OCT3/4) Identifies Cells with Pluripotent Potential in Human Germ Cell Tumors.Looijenga LH, Stoop H, De Leeuw HP, De Gouveia Brazao CA, Gillis AJ, Van Roozendaal KE, Van Zoelen EJ, Weber RF, Wolffenbuttel KP, Van Dekken H, Honecker F, Bokemeyer C, Perlman EJ, Schneider DT, Kononen J, Sauter G, Oosterhuis JW.Pathology/Lab. for Exp. Patho-Oncology [L. H. J. L., H. S., H. P. J. C. d. L., A. J. M. G., J. W. O.], Pathology [H. v. D.], Josephine Nefkens Institute.Human germ cell tumors (GCTs) may have variable histology and clinical behavior, depending on factors such as sex of the patient, age at clinical diagnosis, and anatomical site of the tumor. Some types of GCT, i.e., the seminomas/germinomas/dysgerminomas and embryonal carcinomas (the stem cell component of nonseminomas), have pluripotent potential, which is demonstrated by their capacity to differentiate into somatic and/or extraembryonic elements. Although embryonal carcinoma cells are intrinsically pluripotent, seminoma/germinoma/dysgerminoma cells, as well as their precursor carcinoma in situ/gonadoblastoma cells, have the phenotype of early germ cells that can be activated to pluripotency. The other types of GCT (teratomas and yolk sac tumors of infants and newborn, dermoid cyst of the ovary, and spermatocytic seminoma of elderly) are composed of (fully) differentiated tissues and lack the appearance of undifferentiated and pluripotent stem cells. OCT3/4, a transcription factor also known as OTF3 and POU5F1, is involved in regulation of pluripotency during normal development and is detectable in embryonic stem and germ cells. We analyzed the presence of POU5F1 in GCT and other tumor types using immunohistochemistry. The protein was consistently detected in carcinoma in situ/gonadoblastoma, seminomas/germinoma/dysgerminoma, and embryonal carcinoma but not in the various types of differentiated nonseminomas. Multitumor tissue microarray analysis covering >100 different tumor categories and 3600 individual cancers verified that POU5F1 expression is specific for particular subtypes of GCT of adults. No protein was observed in GCT of newborn and infants, spermatocytic seminomas, and the various tumors of nongerm cell origin. In addition, no difference in staining pattern was found in chemosensitive and chemoresistant GCT of adults. These results indicate preservation of the link between POU5F1 and pluripotency, as reported during normal development, after malignant transformation. Therefore, POU5F1 immunohistochemistry is an informative diagnostic tool for pluripotent GCT and offers new insights into the histological heterogeneity of this cancer.Or are you now going to show us a walking talking individual that has arisen from one of these tumors..which are not caused by a defect in meiosis in any case...nice try salty...try agian

"Please proceed as I am a born experimentalist and look forward to your findings. "M: You are the first born experimentalist I have ever heard of who is unwilling to do the experiments to test his own hypothesis...it is clear to me you have not done a single experiment since the 50's...we look forward to you semi-meiotic experiemental results..or are you admitting you are not a serious student of evolution or a liar ?[This message has been edited by Mammuthus, 05-15-2003]

If you had read my papers, you might know that I have postulated an intermediate evolutionary period in which organisms might simultaneously reproduce both semi-meiotically and sexually.M: Almost forgot...I asked (and so did wj) for EVIDENCE for your assertions...not your postulating....show us a clear example of a population of mammals reproducing sexually and asexually...S: Curiously, there is some evidence for this in humans. Certain ovarian tumors consist chiefly of the ectodermal tissues hair and teeth. Occasionally tumors are found some of which are blond and some brunette in the same female. These can only be explained semi-meiotically with the woman being heterozygous for hair color.M: Please cite a specific example of a mixed color hair dermoid cyst... in any case, hair color mosaicism of a multifactorial trait is hardly surprisingJ Invest Dermatol 1993 Jul;101(1 Suppl):82S-89S Related Articles, LinksHair melanins and hair color: ultrastructural and biochemical aspects.Ortonne JP, Prota G.Department of Dermatology, University of Nice, Sophia Antipolis, France.The color variants of mammalian hair, including spotting and albinism, are the result of melanocyte activity and have been shown to be determined by the action of multiple genes, some of which operate through the milieu in which the pigment cell resides; others appear to act intracellularly to control the type of melanogenesis. Although there has been much descriptive work on the mode of action of these genes, it has only been with the recent advances in the chemistry and molecular biology of melanin pigmentation that some progress is being made in understanding the nature and origin of hair color. It is the purpose of this article to provide an integrated overview of the major advances so made and to draw attention to certain peculiarities of the melanization processes of hair with respect to those underlying skin pigmentation. Key words: melanins, melanocytes, melanogenesis, hair.andJ Am Acad Dermatol 2001 Jul;45(1):136-9 Related Articles, LinksHeterochromia of the scalp hair: a result of pigmentary mosaicism?Restano L, Barbareschi M, Cambiaghi S, Gelmetti C, Ghislanzoni M, Caputo R.Department of Pediatric Dermatology and Center for Inherited Cutaneous Diseases, Institute of Dermatological Sciences of the University of Milan, IRCCS Policlinico, Italy.Five patients who presented stable bands of hair of a different color with respect to the surrounding hair are reported. In 4 patients this was an isolated finding. One patient also had diffuse linear skin hypopigmentation and other abnormalities. We hypothesize that these 5 cases represent a distinct type of hair heterochromia, possibly because of somatic mosaicism for genes affecting pigmentation.and what is the big deal about tumor cells being heterozygous?...many are polyploid...sheesh..this stuff is not so difficult salty.But given your definition of expert you gave to Scott...nobody considers you an expert.

Nice try M but the fact remains that the only way a blond and brunette teratoma could occur in a single female is if the tumors were produced semi-meiotically. Of course there are no walking talking semi-meiotic products. Don't you yet realize that macroevolution (semi-meiotic evolution) is finished? Once again you demonstrate that you have not read or comprehended, probably because you choose not to. salty

M what has scalp hair got to do with ovarian teratomas anyway? I am getting very tired of your nasty comments. They are in very poor taste, but that seems to be a hallmark of this forum. salty

M it must be you that is a liar or you haven't (again) bothered to review my vitae. I published three papers in the journal SCIENCE since the 50's. How many have you placed in that prestigious journal? You see I don't have to remain anonymous. Go to my home page and you will see that I let it all hang out. I don't even know who you are nor do I care. It is you who is incredible. salty

Nice try M but the fact remains that the only way a blond and brunette teratoma could occur in a single female is if the tumors were produced semi-meiotically.M: The data say exactly the opposite (as you have ignored). Exactly the same thing happens with mosaicism of skin color...similar occurences for other traits due to skewed X inactivation...there is nothing semi-meoitic about the data other than your assertion...go back to the dunce corner..try again (maybe read the papers while you are at it).S: Of course there are no walking talking semi-meiotic products. Don't you yet realize that macroevolution (semi-meiotic evolution) is finished?M: Based on what supporting evidence? Why are you holding it back if you actually have it?S: Once again you demonstrate that you have not read or comprehended, probably because you choose not to.M: Once again you have demonstrated you have not read anything in a long long time and can only repeat your assertions like a mantra...

If you do not see the connection between hair development and teratomas then you are truly dense....I really don't care if you are tired of my comments. I am tired of your unsupported assertions and your complete lack of good faith effort to address rebuttals of your points...live with it.

I have been to your homepage and I have seen your list of publications..none of your Science papers are relevant to the topic of evolution....and they are so old that they are not even in Medline!...what the hell have you been doing academically since the 60's?..nothing it would seem..especially for a self proclaimed born experimentalist (agian are you a liar?) since you don't care who I am then I see no need to reveal my identity on an internet forum and then get email spammed by people like you.S: It is you who is incredible.M: Flattery will get you nowhere Your last three posts have been pure evasion of the outstanding questions posed to you by wj and myself.....now get to work and actually answer them ..preferably without the 2 year old child tantrum rants and two sentence handwaving away data you don't like..[This message has been edited by Mammuthus, 05-15-2003]

Nice try M but the fact remains that the only way a blond and brunette teratoma could occur in a single female is if the tumors were produced semi-meiotically.M: Oh yeah..in addition, do you then claim that agouti moust coat color mutants, calico cats, and domesticated cattle (Bos taurus) coat color variation is all a result of semi-meiosis?...rather simple to get two colors in a single diploid individual....

I have a Calico cat. What's the story? As I understand it, all Calico's are female.Moose

Hi Moose,calico's don't have a uniform coat color i.e. the hair is in different color patches.:J Hered 1973 Sep-Oct;64(5):272-
Male tortoiseshell and calico (T-C) cats. Animal models of sex chromosome mosaics, aneuploids, polyploids, and chimerics.Centerwall WR, Benirschke K.The point being, females with two X chromosome shut down one of the two chromsomes randomly during early development to compensate for having one extra X chromsome than men (you know it would not be fair otherwise )If you have color determining genes in a heterozygous state on the X, because of random X inactivation, the individual will be mosaic...and imagine..all this without semi-meiosis....This is irrelevant to the males because with a single X chromosome they will have a uniform coat color...well other than some mutatant malesCenterwall WR, Benirschke K. Related Articles, Links
An animal model for the XXY Klinefelter's syndrome in man: tortoiseshell and calico male cats.
Am J Vet Res. 1975 Sep;36(9):1275-80....this is a case where chromosomal non-disjunction leads to XXY instead of XY male cats which then need to dosage compensate for the extra X they are carrying around....again..all without semi-meiosis...cheers,
M

Here is another paper on mosaicism that is not sex linked...there are lots of ways to have a mosaic appearance in both skin and hair colorProc Natl Acad Sci U S A 1997 Feb 4;94(3):890-4 Related Articles, LinksInherited somatic mosaicism caused by an intracisternal A particle insertion in the mouse tyrosinase gene.Wu M, Rinchik EM, Wilkinson E, Johnson DK.Biology Division, University of Tennessee-Oak Ridge Graduate School of Biomedical Sciences, 37831-8077, USA.A recessive, fully penetrant mutation (c(m1OR)) at the mouse albino locus that results in coat-color mottling has been characterized at the molecular level. Restriction mapping and DNA sequencing analyses provide evidence that mutants carry a 5.4-kb intracisternal A particle (IAP) element insertion upstream of the tyrosinase (Tyr) promoter. Northern blot analysis and reverse transcription-PCR results show that the tyrosinase gene is expressed at much lower levels in mutant than in wild-type mice. The mutant Tyr gene still retains the tissue-specific expression pattern, and the Tyr transcript is not initiated from the IAP long terminal repeat promoter. We propose that the IAP insertion isolates the promoter of the tyrosinase gene from upstream cis-acting regulatory elements, leading to a substantially decreased level of Tyr gene expression in mutants.

I gotta admit, O Tusked One, it would never in a million years have occurred to me to look up a refereed article on cat fur color. (Of course, one possible explanation for that failure is that I hate cats.) Anyway, I am totally awed by your ability to find relevant articles on any subject.

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Outofdate:
Scott, if I understand you, you are no longer certain that I am completely incompetent and now find it necessary to solicit the opinions of experts in the evolution field?

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You do not understand at all. I know you are largely incompetent, and this asinine mantra about population genetics is just one of many examples. I need not solicit opinions, for I know you are wrong. No, I just mentioned that I might forward along some of your more laughable claims to ilicit responses that you might actually pay attention to. On further reflection, however, that would be a waste of everyone's time, as you have no intention of listening to, much less aceepting, reasoned discourse.

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I checked out http://www.arn.org and sure enough my work has aroused some interest there. I find it very revealing that you must denigrate Bertha. She seems pretty rational to me.

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Bertha is a simple-minded stooge. She continues to insist that "directed mutations" occur, despite having dozens of papers cited and having it explined to her dozens of times that they do not. Every week or so, she just reposts the same assertions. just like you. And this is nothing new - I first encountered her probably 6 years ago on the old Internet Infidels board. She made the same refuted arguments then that she does now. She claims to just be 'skeptical' that "RM&NS" can account for extant diversity. yet she is not skeptical at all of any fly-by-night nonsense that roplls along saying otherwise. In fact, she was the one that first linked to your site a few years ago.
Peas in a pod, so to speak.
Oh, and as far as 'generating interest' goes, I did a search for "semi-meiosis" and found only these two threads. It is funny - the only folks that seem to think you are onto something are three people thast have admitted they know nothing of science - mturner, Bertvan, and jazzraptor - and a handful of simpletons who jump on any bandwagon they can. And there, like here, many of the flaws in your 'thinking' are pointed out. An interesting quote from an evolutionary biologist/entomologist:

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"Apart from that, his essay reveals little to me other than that the guy's a crackpot. For example, he discusses the issues that sexual reproduction presents for evolution, yet he shows no sign of having read anyone's research on the subject, despite the mountains of both theoretical and empirical work that have been done. I am not even certain that he is aware that it exists, and he certainly doesn't seem to be aware of the mathematical simulations that do exactly what his statements claim are impossible.

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He talks about chromosome rearrangements being involved in the creation of new species (giving humans as an example). Yet he does not mention *any* of the work done since the 1982 paper he cites that shows how chromosome rearrangements can occur without speciation, or how speciation can occur without chromosome arrangements, or even some of the very recent work that provides some positive support for his position. Again, I doubt he read any of it, or is aware that it exists. The guy is simply out of touch with an enormous body of scientific research which is relevant to the points he is trying to make, and that does not engender much confidence. "

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if that is what you mean by "generating interest", well, so be it.

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By the way an expert is nothing more than someone who has convinced others that his judgement is superior to theirs.

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If you say so.

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Dawkins, Gould, Mayr, Futuyama and Provine come to mind.

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not to mention Bateson, Goldschmidt, Broom, and Grasse. Throw in some arrogance and call it a winner.

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A few years ago I had correspondence with Ernst Mayr which terminated when he reminded me of how many thousands of words he had written on the subject of evolution. At least he responded which is more than I can say for Gould down the hall. I predict you will get very little response from any real students of evolution. Please proceed as I am a born experimentalist and look forward to your findings.

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That appears to be a lie. You have done no experimentation whatsover for more than 10 years, certainly notihng to test your hypotheses. Asserting something does not make it true.
As for Mayr and Gould, here is a little anecdote that I presented once before when a similar subject came up (Borger whining about not getting replies from real scientists).My graduate advisor is considered one of the world's leading experts on the molecular evolutoin in Primates. When I was a graduate student, I would sometimes pick up his mail from the department office and deliver it to him. One day, he received a post-card form one Kelly segraves - who, if I recall correctly, is or was a well-known creationist activist. The post card had some nonsensical ramblings about dinosaurs and such, and asked some questions of my advisor. He chuckled to himself, showed it to me, then threw it in the garbage.
One can only guess that Segraves, after not hearing from my advisor for several weeks, 'concluded' that my advisor simply could not handle the questions and that he, segraves, was right.[This message has been edited by SLPx, 05-15-2003]