Minnetonka Boot Black How To Wear

CONVERSATORIO SOBRE PRIVATISACION DE SAN MARCOS

Los invito a asistir at a meeting on privatization of San Marcos
Venue: School of Biological Sciences.
UNMSM Time: Thursday July 22 at 5 pm. Sincerely


Luis Arbaiza
biologist with a major in genetics

UNMSM
dnarb9000@yahoo.com
http://luisarbaizaescalante.blogspot.com/2010/06/un-san-marcos-sin-pobres.html

First we must remember that talk about the best university in Peru, or perhaps the least worst, as determined by the International Institute for Higher Education in Latin America and the Caribbean (IESALC), Unesco

and the National Assembly of Governors (ANR).

How is college without money (this year were removed for good three quarters of the money he received in a country which claims to be more and more rich), violence, lack of laboratories and facilities, structural problems, violent groups, fascists and a serious political and administrative corruption can be the best?
The answer is the students.
The casting more rigorous in the country and many countries around give or gave the best students.
Well, all of San Marcos are good students, but that's enough.

Some, many authorities now in San Marcos, wish to privatize it. This article
refute the arguments for privatizing

Some argue that if private outside San Marcos would be no order, no labor disputes, political zero, good bathrooms, etc control. There would be chaos and violence.

suggest sacrificing the poor students to achieve this end and have a more tidy and organized university. San Marcos would then be a place where the poor would be a tiny minority (if they exist) as in the private universities (Cayetano, San Martín, Catholic), which is rare and difficult to be poor. For private universities is exercised over terrible discrimination to young people: if you are poor, do not enter or if you go, study will be much harder for you, if you're broke.

These people are worried about San Marcos but not by their estudiantes.Olvidan, or do not know, that a university is not an end but a means. The end are the students and the environment are the facilities, infrastructure, staff, authorities, libraries and baths.
San Marcos is a machine with an end, the goal is to produce knowledge (no money) and second professional. Everything should be built for it. The building serves students not students at the building. Just as a hospital is for patients and not for medical or building.
To get a better university must be better managers.
Others think that Mark should be privatized because there is no money, the state gives less and less, there is no where to raise the salaries of teachers, who San Marcos should be making money. Then the money must come from students and poor students are not where them out. Conclusion privatize for young people with more money coming. This reasoning is like a father to his children ask for money to raise them. Or as a parent who thought their children should make money and raise him.
Universities are not businesses, are not kiosks whose mission is to make money, profits. Its purpose is to produce knowledge and professional.
For more money, students and government authorities should require, stop it and there are state taxes paid.
Others say that Mark should be privatized to make it better academically, but San Marcos is now the best academically and all universities and universities in the ranking of Peruvian private universities are generally the worst. And the best national, as elsewhere in the world.
In most private universities, the intellectual level is extremely low, students are seen as people who gouge and not educating, teachers are required to lower the level of classes to "keep the client" (as I said an authority on San Martin where he founded a chair, refusing to do so and to agree to a student who had not attended any kind of laboratory mean not hire me again.) The entrance exams do not test anything, comes either, if that many students go disapproved, becomes "bell" bone in the middle with more paper passes, and are all frowned upon and ensure students enrolled in the next cycle and help your business thrive.


Others think that Mark should be privatized so that terrorist groups do not arise as a path or MRTA in the 80s, this argument is fallacious because terrorist groups do not arise by the mere existence of public universities, if so, will emerge in public universities as
Cambridge, Oxford, Berkeley, UCLA, the Sorbonne in Paris. Complutense de Madrid, Salamanca, UANL and much more.

The way to avoid the emergence of these heinous doctrines such as trail or MRTA is the welfare state. A society in which the economy serves the human beings (all) and not human beings on the economy. Terrorist groups live "sharpen the contradictions", reduce the disappears. Another essential ingredient of doctrines how are you is religious fanaticism, dogmatism and irrational. The sound education anti-dogmatic and anti-conservative is the best antidote. SAN MARCOS

AND PRIVATIZATION IS A MEDIUM
All graduate already privatized. It is impossible to be poor and do a Masters in San Marcos for their high costs, like salary with a Peruvian family living average.
The pre-San Marco academy costs about 600 soles a month. So in the PRE are also excluded the poor.


unfairly can reserve a percentage of vacancies for these privileged students. For those who are normal examination (ultra hard) is now more difficult to fight for fewer vacancies because many are reserved for the wealthy students of PRE.
So join San Marcos is easier if you have money. Pre-san
frames should not exist or your students should take the same exam as everyone else.
The very poor do not exist in San Marcos, dry the poor will soon be a minority in San Marcos, as if the poor were a minority in Peru! San Marcos
the country should play in the role played by the cerebral cortex in the human body, dreaming the universe unravel the nature, understand the man, create and explore the beauty and art. Anyone with enough brains, but not enough pockets, you should have the opportunity to make a difference in the story of his life and the country. All born in Peru should be entitled to be happy. And education is one of the most beautiful forms of happiness. As in my generation that thousands of poor students did San Marcos and change our lives.

But it will not. San Marcos is condemned to be blind and unconscious body, and perhaps vestigial if those who can not decide to privatize rather disappear or shrink as much as possible. It will be like those sad universities ultra clean bathrooms and equipment where there is no intellectual gatherings or philosophical discussion, no art, no real science. A place to study only the children of the owners of this, that they alone are the masters of the future and the country. Or where careerists achieve a better social status. The San Marcos
we love is disappearing and instead stay on a superficial and ignorant impostor.





Here is a short list of intellectuals who were from poor backgrounds:


Einstein (son of a mattress)


Newton (son of peasants)


Dickens

Socrates


Sabato


Saramago


Dostoevsky

Miguel Angel


Aesop (slave)

Bose (quantum physics)

Riemann


Epictetus (slave)

And what?


Did someone let him be tomorrow?



Luis Arbaiza
Biologist with a major in genetics

UNMSM dnarb9000@yahoo.com
http://luisarbaizaescalante.blogspot.com/2010/06/un-san-marcos-sin-pobres.html
If
inquire about this text, "Please put some copy and distribute it. If you greet
Internet, forward it to those who want more

Big Older Women Girdles

BIRTHDAY WITHOUT POOR Pythagorean rotation a dark, year after year, leaves me somewhere in the world ... Ambiguous



arduous lso students knew what the Pythagorean
the stars and men become cyclically.
not know if I'll in a second cycle,
but a dark rotation
Pythagorean yra year I left a place in the world ... Borges.

How To Beat The Game Of Poptropica

REPORT ON THE CAUSE OF BEARS


Ambiguous REPORT ON THE BEARS

When there are difficulties in defining a category (for example, that is a bear) are only two possible things: either the category does not exist or exists but nobody has yet sound in words. For
I think it bears passing second.
A category must be universal and essential. And so it must be so the bears. Being

bear is related to many physical and behavioral traits, etc but all are related to a cause that gives rise to that collection of traits. Being
bear is identified with the ideal of what being a man in a biological sense. Be Bear is not a cultural accident of an era but a universal and transcultural vision of being a man.
The emergence of culture in the 70s do not like many believe a rejection of cultural stereotypes of what being gay (basically being a man playing a woman) but a return to the conception of themselves as men in the biological sense , not cultural. Innate and not learned.
What we consider beautiful in the sexes is conditioned by two ingredients, a cultural (different and accidental) and other biological (innate and essential).
So women are considered universally beautiful if they are younger, if you have wide hips and reproduction traits associated developed. These are desirable traits for an evolutionary logic-breeding of the species. Younger women are more fertile so.
evolutionary logic is same-reproductive when applied to men as an ideal biological gives the type bear. So we can say that being a bear is to be an ideal man (no eye in the cultural sense)
This can only cause broken down into 3 implications. 1 .- First
testosterone and its effect on the male anatomy gives much of many features considered beautiful on the bears. Muscles, masculinized appearance, body hair, strength. 2.-
overweight is considered in the nature of evidence of benefit in access to resources. And is the source of that experience as beautiful. 3 .- Finally
age is a determining feature in feminine beauty, is not in the male to not be so related to reproductive capacity.

These three elements with a common origin give explanation to the image of the bear. And you can contrast with the stereotyped and alienated from gay identity is female anatomical criteria: young men, whether male secondary sex characteristics, and slender.

But the approach, let us say it sounds weird, neo-Darwinian than it is to be bear as:
Fat, hairy, hairless, male, leathers, assets, liabilities, modern, versatile, young guys, informal, bald black, white, cholos, Eastern, Latino, European, American, Asian, etc, etc. And do not
would be: thin, ladies, crossdressers, hairdressers, fashions.


Apart from this being a bear does not mean anything else. Neither self-acceptance, and visibility or sexual orientation. Being
bear is just a state of body. Luis Arbaiza

Ap Biology Population Genetics

IMPRINTING IN HUMAN GAMETES






THE CAUSE OF IMPRINTING IN HUMAN GAMETES
Luis Arbaiza
UNMSM

1 .- INTRODUCTION

A sperm and an egg are genetically identical, but epigenetically different.
This difference is called imprinting. Having a maternal and a paternal imprinting.
The union of two gametes, one maternal and one paternal imprinting allows normal development of the embryo.
The imprinting means that certain genes, involved in this process, are turned off or pinned by a typical pattern and standard, depending if in the sperm or the egg mature.
genes that are turned in a gamete are off in the other gamete. And this makes
functionally different. In general, the genes expressed in the parental imprinting elevate fetal development while it limits the maternal.
(Paolini 2004)


The union of gametes with the same imprinting, leads to different epigenetic defects and embryonic development unviable.
The immaturity of this process cam epigenetic defects.

But what causes et epigenetic difference?
still can not completely answer this question.

The motivation for this research literature is to develop a hypothesis about the cause of imprinting and perhaps find experiences that support this hypothesis experimentally. JUSTIFICATION


genetic imprinting is a prerequisite for normal development of embryos
As this takes place in the germ line, the error must carry errors that prevent the successful development of embryos.
Especially in ICSI procedures such as those that "jump" steps of epigenetic processes in the male gamete.
This could explain why it has been shown greater percentage of epigenetic diseases in children conceived with ICSI
and nurse found that defects in the methylation of the H19 gene and MEST in oligozospermicos (CJ Marques 2008) This might also explain the increased occurrence of Silver-Russell syndrome in children with hypo-methylation of the H19 gene ART born. (CJ Marques 2008)


addition, a low methylation of the binding site could lead to inactivation of the paternal IGF2 gene and linked to low embryo quality and low weight, often associated with ART (artificial reproduction thecnologuies). (CJ Marques 2008)

3 .-
For delimitation of the problem to develop a hypothesis about the cause of imprinting must travel several areas still poorly investigated this phenomenon, which can be grouped investigations that respond to certain questions, none with a complete and sufficient answer:
genes
3.1 What are these?
3.2 When you change?
3.3 Who the changes? 3.4
how the changes?
3.5 What is the uncaused cause of imprinting? Is it genetic or epigenetic?
3.6 What is the relationship with the Sry gene which is obviously the only difference between male and female genome, and uh be the starting point of this differentiation? MATERIALS AND METHODS


literature was analyzed in subjects related to try to answer the research questions to what was agreed virtual libraries and software for data management and virtual communication with researchers in the area. RESULTS



3.1 WHAT ARE THE GENES?
A genome imprinting, about 156 potential new genes, and imprinting status-gene can be predicted by its sequence (Luedi, PP et al. (2007). The classic mechanism of genetic imprinting is a gene methylation but is not the only and does not necessarily mean inactivation.
Here is a list of some genes known as imprinting involved in the human.

State Chromosome location GEN sperm into the egg state active role 1 NOEY2

active (tumor suppressor)
active IGF2 Independent control of others, the change carries many more
7p12 genes (GRB10) in growth factor receptor protein PEG10 10
7 q21 active inactivated may be a new gene imprinting
7q31.3

MEST isoforms 1 and 2, 8 KCNK9
(active in the brain causes cancer, bipolar and epilepcia)
DLGAP2 8p23 (possible bladder tumor suppressor)
DLGAP2
associated protein-2 (Dlgap2). WAS
Excluded as the gene responsible for EPMR.
11
inactive H19 noncoding RNA active role in cancer

a member of the AP2 transcription factor family

Transcription factor E2F1 may uan

different from control of others
His other genes change more
drag
11 p57, Kip2 CDKN1C active
MEG3
14 q, 15 q11-q13
active SNRPN (small nuclear ribonucleoprotein, polypeptide N) 15 q11-q13
IPW functions not
polypeptide RNA. Predominantly in brain

15 Causes UBE3A Angelman syndrome. on the mother's chromosome 19q13.4
passkey
Possible active XIST
inactive X
Idica that methylation is removed in spermatogenesis Xist (is in mice)

NESP55
ATP10A
PHLDA2

MAGEL2
SNRPN NDN
inactive PEG3

CDKN1C KCNQ1
KCNQ1OT1
TP73
IGF2R
WT1
SLC22A18




3.2 What HAPPENS WHEN IMPRINTING?

During the development of primordial germ cells imprinting pattern is deleted. Likely to enter the gonad. SPERMATOGENESIS



Completes in the haploid phase (meiosis) in man before meiosis occurs as soon as when spermatogonia proliferate, according to some authors is intrinsic and cell-Autonomous. Oogenesis


ocytes The imprinting occurs around the time of the first division meiotic, methylation occurs in women in the postnatal development when ooccitos are diplotene prophase I, the maternal imprinting continuously established in the maturation of oocytes.

But methylation may be at different times for different genes (Paolini 2004)

has been found not due to the influence of somatic cells of the genital ridge or gonad environment in primary cells. (Paolini 2004)



IMPRINTING AND DEVELOPMENT STAGE TIME Time IMPRINTING STATUS OF SPERMATOGENESIS oogenesis
0 Zygote

exaggerates the imprinting DIFERENCAI
demethylated paternal methylation shortly after fertilization, the mother undergoes de novo methylation
4 hours
In mouse paternal pronucleus is demethylated within 4 hours after fertilization

4 hours
A global demethylation occurs in the morula at 4 h of fertilization .



5 days
In the blastocyst restores methylation in the inner cell mass but not in the trophectoderm. In the blastocyst reestablesce methylation in the inner cell mass but not in the trophectoderm. (Kierszenbaum AL. 2002)


MASH2 regulates the development of spongiotrophoblast
Igf2 has been found in labyrinthine trophoblast expresses
ASCL2 spongiotrophoblast and labyrinthine in 3-4 weeks

as PGCs Primordial germ cells have migrated paternal and maternal imprinting The Primordial germ cells inherit a biallelic imprinting father and mother, and delete your imprinting to start a de novo during gametogenesis. (Kierszenbaum AL. 2002)
primordial germ cells expressing these genes: Blimp1, Oct3 / 4, Fragilis, Stella, c-Kit, MVH, DAZL and Gcna1 (Deshira Saiti 2000)


H19 and Igf2 are expressed in endoderm and mesoderm (Andrea L. Webber January 1998)

6 weeks Embrionic
germ cells have no imprinting or is deregulated, and gonad are primordial cells
40 are intended to be gonad Exra-induced tissue embryonic cells is hypothesized that somatization stifle
Blimp1 program (or Prdm1), a repressor that foundation helps tarscripcion (Yasuhide Ohinata 2005)


at birth and within months is completed Parental imprinting
esperamatogenesis puberty started. The paternalisacion is an ongoing process in-Dividing mitotically and meiotically spermatogonial stem cell-derived progeny Dividing spermatocyte (Kierszenbaum AL. 2002)
Dnmt3L and Dnmt3b interact with Dnmt2a and Dnmt3b and is required for proper spermatogenesis. (Kierszenbaum AL. 2002)


MATURITY The imprinting is already mature in the stem cell line in germinal (CJ Marques 2008)

Spermatogonia are immature germ cells do mitosis
Some differ to primary spermatocytes.
After the first meiosis spermatocytes become secondary
2

These are meiosis 2 and form 2 spermatids





Spermatogonia (diploid) are in speramtozoides already methylated H19

THE AMENDING 3.4 Who?

to imprint genes are usually methylated in its promoter, making them inactive. (Methylation is the addition of a methyl group on a Carbon nucleotide)
methylation silencing is not always
Methylation chromatin structure changes
A pattern of methylation is the result of: 1 .-
de novo methylation maintenance

2 .- 3 .- demethylation
(Paolini 2004)



promoters imprinting genes are rich in CpG islands

The enzymes that make this methylation are 3 DNA methyltransferases, DNMT 1


Dnmt3a Dnmt3b

For example DNMT 1 catalyzes the transfer of a methyl group (CH3) from S-adenosylmethionine (SAM) to carbon 5 of cytosine resulting in a 5-methylcytosine.
unmethylated
These islands are susceptible to bind to proteins (eg MECP2 "methyl CpG-binding protein 2)

Dnmt3a and Dnmt3b are de novo methylation Dnmt1
when divided by a new DNA methylation in the daughter strand

The demethylation occurs in the absence of Dnmt1 with continuous cycle of DNA replication (passive demethylation) but also active (no DNA replication .) The nature of the demethylases is still unknown. Dnmt3L

assists

novo methylation of Dnmt3a and Dnmt3b appear to be the giving patterns of methylation in the early embryo
DNMT1 is what keeps this pattern of mother cell to daughter (two copies)

3.5 What is
CAUSE NO CAUSE OF IMPRINTING?

Presumably because imprinting genes are numerous (perhaps hundreds), and not all are modified simultaneously, there is a cascade of reactions that leads this change gradually until fully matured.
bibliographic information realizes certain stages of this cascade could not envision the total trigger of this phenomenon. Although it is reasonable to lift the absence or presence of sry gene, single gene that differentiates male and female genomes, and ultimately determine gametogenesis and oogenesis.


FRAGMENTS OF MATURATION PROCESS OF IMPRINTING


cause consequence
KCNQ1OT1 The expression of the gene on chromosome 11p15.5, is essential for the imprinting of certain regions. The mechanism may be a gene is active in a ovarian or spermatic say this cascade occurs in other imprinting genes.
studying their transcricion factors could be achieved by knowing what the root cause of imprinting

IG-DMR The ergenic germline-derived differentially methylated region (IG-DMR) is candidatopara control region of chromosome 12
is a cluster that contains:
paternally Expressed protein-coding genes Dlk1 and DIO3 and several non-coding RNAs, including maternal expression of Gtl2 and C / D snoRNAs.
A retrotransposon-like gene (Rtl1) is Expressed from the paternal chromosome and has an antisense transcript from the maternal chromosome Expressed containing two microRNAs with full Complementarity to Rtl1

Deletion of IG-DMR of the maternal chromosome causes loss of imprinting on all cluster genes
The deletion leaves intact paternal imprinting

19q13.4 Some women do not have a piece of chromosome: 19q13.4 and its imprinting pattern in their eggs is paternal


EXPERIENCES GIVING EVIDENCE ON THE CAUSE OF INDIRECT
IMPRINTING Experiments conducted with other aims at finding the causes of imprinting can provide experimental evidence on some aspects This
Their analysis may lead to you hypotheses and / or indirectly sustain
experimentally
EXPERIMENT MOTHER OF 2
In 2004, Japanese researchers obtained mice female offspring of two mothers.

The zygote genome did so with a mature and an immature (Tomohiro Kono 2004) The oocyte was not developed a mouse mutant with a deletion of 13-kilobase
The undeveloped is (ng)
and development (fg)
But in the ng was not altered
H19 and Igf2 H19 To block ng was used in a mouse with a deletion in the gene
The embryos were born to 17.5 days
was confirmed that these embryos do not spend the day 17.5
The 2 were born growth retardation had a poorly developed liver Igf2 and H19
As Dlk1 and Gtl2 are printed on spermatogenesis.

From this we can conclude that the maternal methylation occurs in oocyte maturation and the Occitan immature sperm is homologous to epigenetically speaking.
And, on the other hand the imporntin of H19 and Igf2 genes is independent and find their cause in the region of 13-kilobase

IMPRINTING Modification

Some substances such as synthetic estrogen, diethylstilbestrol (DES) can turn DNA methylation pattern. (John A. McLachlan, 2001)
The expression of imprinted genes and fetal development is influenced by the addition of fetal calf serum culture medium (Paolini 2004)
is not known how this medium affects the imprinting Perhaps
removes methyl groups, leading to incomplete or delete the pattern of imprinting. (Paolini 2004)


E IMPRINTING
ICSI ICSI Children weigh less (Paolini 2004)

EXPERIMENT
First female sperm stem cells turned into sperm that impregnated
(Nayernia K 2006)
marrow cells were transformed into male germ cells were expressing germ cell markers (Nayernia K. 2007)
born mouse had defects and will use special chemicals and vitamins
PRODUCER OF SPERM WOMAN

A idatiformes molas locus 19q13.4. Examined the methylation the daughters and the mola
The mutation is inherited from the grandfather or maternal grandfather so we conclude that the error is not due to an erased imprinting marks if not quite the re-establishment of native brands in oogenesis or in post-cigotic maintenance (El-O Maarri 2003)


CONCLUSION This analysis has been able to generate hypotheses
síguete

HYPOTHESIS Two mutually independent mechanisms that initiate the cascade of events leading to the pattern of paternal or maternal imprinting .
1 .- A gene in 19q13.4 is responsible for feminizaría a significant number of genes to print
And another alter H19 and Igf2


DISCUSSION There are apparently two mechanisms locomotive upon which the imprinting of these mechanisms must be related to the presence or absence of SRY but that relationship is still nebulous.
is known that some methylating enzyme is responsible for imprinting genes, these genes also are rich in CpG islands but because in a gamete are methylated and not in another, still the same question arises how this enzyme known to methylate genes and which are not? And as you know when methylated if a sperm or an egg. Some of these enzymes also signal a different or activates these enzymes

The mechanism may be a gene is active in a ovarian or spermatic say this produces cascade to other imprinting genes.
abortions should study what ICSI and art to see how they are epigenetically by altering these techniques the normal maturation of imprinting in the gametes. There is already evidence of increased disease epigenetic ARTs cup
Deletion of IG-DMR of the maternal chromosome causes loss of imprinting on all cluster genes that marks it as a locomotive gene imprinting.
The deletion leaves intact the parental imprinting
Some women do not have a piece of chromosome: 19q13.4
This healthy gene feminizaría eggs.
sperm could feminize H19 and Igf2, apparently, are printed by a mechanism independent of this. If
achieved the correct expression of IGF2 and ha19 a large number of other genes is well placed (maternal bone becomes father)
The experiment of mice with two mothers can deduce the following:

"We conclude that an immature oocyte and sperm except for 2 genes (IGF2 and H19)
-one was nullified (h19) to get the sperm
-hence a sperm is like an immature oocyte except for 2 genes
"If add the egg maturation factors and vanishes IGF2 could turn sperm into eggs.

weigh less ivf Apparently, that talks about winning the bony maternal genes that paternal genes are incomplete
WOMEN PRODUCERS
MDE SPERM

If there is a mutation that makes the maternal genome paternal
1 .- A simple element determines parenthood
2.-genome that healthy gene feminizaría sperm. 3 .- partenisación
genome requires no activation or suppression of this gene or factor.
The normal state is paternal
may first have to delete and then print
We hypothesize that the factor of follicular development as well as IGF2 gene silencing can change the parental imprinting of the sperm mother




Arie Look
BIBLIOGRAPHY l1, Edward Robinson2, John R. McCarrey2 & Howard Gamete−specific methylation correlates with imprinting of the murine Xist gene Nature Genetics 9, 312 - 315 (1995)

Arie Mira l1, Edward Robinson2, John R. McCarrey2 & Howard Cedar1 Gamete−specific methylation correlates with imprinting of the murine Xist gene Nature Genetics 9, 312 - 315 (1995)

C.V. Beechey GENETIC AND PHYSICAL IMPRINTING MAP OF THE MOUSE
and B.M. Cattanach Mammalian Genetics Unit, Harwell, Didcot, Oxon OX11 ORD, UK

El-Maarri O, Seoud M, Coullin P, Herbiniaux U, Oldenburg J, Rouleau G, Slim R Maternal alleles acquiring paternal methylation patterns in biparental complete hydatidiform moles Hum Mol Genet 2003; 12:1405-13
2003

El-Maarri O, Slim R Familial hydatidiform molar pregnancy: the germline imprinting defect hypothesis? Curr Top Microbiol Immunol 2006; 301:229-41 2006

Horsthemke, B Gerald F. Bai-Lin Wu,1,2 and Bernhard Horsthemke5Charité, Am J Hum Genet. 2002 July; 71(1): 162–164. Intracytoplasmic Sperm Injection May Increase the Risk of Imprinting Defects

Kaomei Guan1,4, Karim Nayernia2,4, Lars S. Maier1, Stefan Wagner1, Ralf Dressel3, Jae Ho Lee2, Jessica Nolte2, Frieder Wolf1, Manyu Li2, Wolfgang Engel2 & Gerd Hasenfuss Pluripotency of spermatogonial stem cells from adult mouse testis Nature 440, 1199-1203 (27 April 2006) 2006

Kierszenbaum AL. Genomic imprinting and epigenetic reprogramming: unearthing the garden of forking paths. 2002
Mol Reprod Dev. 2002 Nov;63(3):269-72.

Lin SP, Youngson N, Takada S, Seitz H, Reik W, Paulsen M, Cavaille J, Ferguson-Smith AC. Asymmetric regulation of imprinting on the maternal and paternal chromosomes at the Dlk1-Gtl2 imprinted cluster on mouse chromosome 12. 2003Nat Genet. 2003 Sep;35(1):11-2.

Luedi, P.P et al. Computational and experimental identification of novel human imprinted genes. (2007) Genome Res 17:1723-1730].
Manning Martina a, Willy Lissensb, Wolfgang Weidnera, Inge Liebaersb DNA Methylation Analysis in Immature Testicular Sperm Cells at Different Developmental Stages
Vol. 67, No. 2, 2001
MANNING Martina; LISSENS Willy ; LIEBAERS Inge ; VAN STEIR TEGHEM André ; WEIDNER Wolfgang ; Imprinting analysis in spermatozoa prepared for intracytoplasmic sperm injection (ICSI) International journal of andrology
2001, vol. 24, no2, pp. 87-94 (17 ref.)

McLachlan John A. , Mathew Burow, Tung-Chin Chiang and Shaun Fang Li
Gene imprinting in developmental toxicology: a possible interface between physiology and pathology 2001 Toxicology Letters
Volume 120, Issues 1-3, 31 March 2001, Pages 161-164

Marques C.J. 1, P. Costa1, B. Vaz1, F. Carvalho1, S. Fernandes1, A. Barros1,2 and M. Sousa Abnormal methylation of imprinted genes in human sperm is associated with oligozoospermia2008 Molecular Human Reproduction 2008 14(2):67-74;

Nayernia K. Drusenheimer N, Wulf G, Nolte J, Lee JH, Dev A, Dressel R, Gromoll J, Schmidtke J, Engel W, Putative human male germ cells from bone marrow stem cells. Soc Reprod Fertil Suppl. 2007;63:69-76.

Nayernia K., Lee J.H., Drusenheimer N., Nolte J., Wulf G., Schwandt I., Ralf D., Müller C.H., Gromoll J., Engel W. Derivation of germ cells from bone marrow stem cells. Lab Invest Volume: 86 Pagination: 654-6632006

Nayernia K, Vauti F, Meinhardt A, Cadenas C, Schweyer S, Meyer BI, Schwandt I, Chowdhury K, Engel W, Arnold HH. Inactivation of a testis-specific Lis1 transcript in mice prevents spermatid differentiation and causes male infertility.
J Biol Chem. 2003 Nov 28;278(48):48377-85. Epub 2003 Sep 16.

Nayernia K.Lee J.H., Engel W., Stem Cell Protein Piwil2 Modulates Expression of Murine Spermatogonial Stem Cell Specific Genes.
Mol Reprod Dev. Volume: 73 Number: 2 Pagination: 173-1792006

Nayernia K, Nolte J, Michelmann HW, Lee JH, Rathsack K, Drusenheimer N, Dev A, Wulf G, Ehrmann IE, Elliott DJ, Okpanyi V, Zechner U, Haaf T, Meinhardt A, Engel W.In vitro-differentiated embryonic stem cells give rise to male gametes that can generate offspring mice. Dev Cell. 2006 Jul;11(1):125-32

Nayernia K, Lee JH, Drusenheimer N, Nolte J, Wulf G, Dressel R, Gromoll J, Engel W.Derivation of male germ cells from bone marrow stem cells.
Lab Invest. 2006 Jul;86(7):654-63. Epub 2006 May 1.

Paoloni Ariane -Giacobino1 and J Richard Chaillet Genomic imprinting and assisted reproduction Reprod Health v.1; 2004


Saiti Deshira and Orly Lacham-Kaplan Mouse Germ Cell Development in-vivo and in-vitro Tomohiro Kono1,3, Yayoi Obata1,3,
Quiong Wu1,3, Katsutoshi Niwa1,3,Yukiko Ono1, Yuji Yamamoto2,3, Eun
Sung Park4, Jeong-Sun Seo4,5& Hidehiko Ogawa1,3 Birth of parthenogenetic mice that can develop to adulthood2004 NATURE for the imprinting of H19 and Igf2 genes199Nature 391, 711-715 (12 February
Yasuhide
Ohinata1, 7, Bernhard Payer2, 7, Dónal O'Carroll3, 7, Katia Ancelin2, Yukiko Ono1, Mitsue Sano1, Sheila C. Barton 2, Tetyana Obukhanych4, Michel Nussenzweig4, Alexander Tarakhovsky3, Mitinori Saitou1, 5,6 & M. Azim Surani2 Blimp1 is a critical determinant of the germ cell lineage in mice2005 Nature 436, 207-213 (14 July
2005)

Rom Pokemon Silver Cheats

LIFE IS

IS LIFE Luis Arbaiza