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Egg donor expenses  2010-09-01 03:54:58

 

The body that regulates fertility treatment in the UK is considering increasing compensation for egg and sperm donors.

Women who donate eggs are currently paid £250, but this could rise considerably under moves to address egg and sperm shortages at IVF clinics.

Many fertility clinics have long waiting lists, driving some childless couples abroad.

No decision will be made until the end of a public consultation next year.

A spokesperson for the Human Fertilisation and Embryology Authority (HFEA) told the BBC: "We will be looking at a number of issues related to donation policies, one of which will be compensation given to donors. We haven't decided on a figure."

The HFEA is holding a three-month public consultation into its donation policies, starting in January 2011.

It follows concern over the number of Britons travelling to countries such as Spain to receive IVF because of shortages of donated eggs and sperm in the UK.

In the UK, egg and sperm donors cannot be paid but can claim "reasonable expenses" for travel and loss of earnings.

This is limited to a maximum of £250 per cycle of egg donation or course of sperm donation.

Some fertility experts say this is too low to attract donors, and they should be paid more for their time and efforts.

Waiting list

Reports have suggested around £800 or more per cycle of egg donation but this has not been confirmed.

Susan Seenan of the support group, Infertility Network UK, which helps infertile couples, said it was right to look at all the policies surrounding egg and sperm donation.

She said: "We know that many patients are travelling abroad for treatment, often because of the severe lack of sperm and egg donors in the UK.

"Although many patients do receive a high standard care abroad, this is not ideal and the rules and regulations in other countries can be totally different from that in the UK."

She said patients deserved access to safe, regulated treatment in their own country, and there was a need to find some way of increasing the number of both sperm and egg donors in the UK.

Via: bbc.co.uk

The Evolution Of Eggs And Sperm  2010-09-01 03:54:31

 

Have you ever wondered why most sexually reproducing organisms have two contrasting sex cells: big, immobile eggs in females and plenty of small motile sperms in men? Scientists have at last disclosed the secrets behind the reproductive science.

James Umen and colleagues at the Salk Institute for Biological Studies in California, examined related algae – the single-celled Chlamydomonas reinhardtii and the multicellular Volvox carteri, which diverged from each other 200 million years ago.



Both types are known to reproduce sexually under certain conditions. While V. carteri reproduces through the fusion of a large female egg and small male sperm, C. reinhardtii's sex cells are of a same size and cannot be categorized as male or female.

The process in each case is controlled by a genetic sequence known as the Mating Locus, or MT, which the researchers hoped would yield clues as to why the sex cells produced by the two types of algae are poles apart.

The researchers compared the MT regions of both algae by examining the RNA sequences produced by each. They found that although V. carteri's genome is just 17 per cent bigger than that of C. reinhardtii, its MT region is five times larger.

Although, some of the genes identified were common to both, the team identified five new genes present only in V. carteri's female MT and eight new male genes.

Crucially, although these are completely new, the team found similar genes with non-sex roles close to the MT area in the genome of C. Reinhardtii. It looks as if Volvox had translocated these genes into its MT area, and over time they have gained new functions related to sex.

"The genes evolve rapidly in sex-specific ways," said Umen, who believes they accumulate mutations over time. A beneficial mutations must have lead to larger eggs and smaller, plentiful sperm.

Via: living.oneindia.in

 


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Mitochondrial DNA remains one of the relatively unknown aspects of human genome to the general public. The word human genome is used to describe the total genetic information i.e. total DNA content in human cells. This includes nuclear as well as mitochondrial DNA.
Human cells contain a nucleus along with various organelles like golgi, mitochondria, endoplasmic reticulum etc. Out of these organelles, mitochondria are believed to have evolved from a primitive endosymbiotic bacteria that entered and co-evolved with the eukaryotic cells. So, these mitochondria also have DNA that resembles the DNA of primitive cyanobacteria but has undergone tremendous changes because of its evolution inside the eukaryotic cells. During this period, the nuclear DNA of eukaryotic cells has also undergone changes to accommodate and utilize mitochondrial resources. So what started as a facultative symbiosis is now an obligatory relationship!

So, human genome consists of both nuclear genome which is about 99.9% of total genetic information, and single mitochondrial genome which is remaining 0.1% of the total genetic information.

Mitochondrial genome is a densely packed small circular DNA duplex. It is around 17 Kb in length and 44% of mtDNA consists of G & C bases. The two strands of mtDNA have different base composition – The heavy strand (H) is rich in Guanine whereas Light strand (L) is rich in Cytosine.

Each cell contains hundreds to thousands of mitochondria in the cytoplasm. Each mitochondrion contains multiple copies of mtDNA. This copy number of mtDNA varies in each mitochondrion and total number of mitochondria also varies from cell to cell, for instance, there are more mitochondria in muscle and brain cells than in skin cells. So effectively, the total number of mtDNA copies may vary extensively depending on the type of cell.

Each human mtDNA contains 37 genes in which 28 genes are encoded by heavy strand, and nine by the light strand. Out of these 37 genes, 24 genes specify a mature RNA product and remaining 13 genes encode polypeptides.

Mitochondrial genome is important as it performs two main functions:
mtDNA provide instructions for making enzymes which are involved in oxidative phosphorylation i.e. an enzymatic process in cell metabolism that generates energy in the form of chemicals called ATP .
mtDNA also encodes tRNAs, rRNAs and some proteins which are used in mitochondrial protein synthesis.
Mitochondria helps in regulating the self-destruction of cells by a process called apoptosis.
Mitochondria may also help in metabolism of certain substances.

It is interesting to see that mitochondrial DNA does not obey the classical mandelian rules of inheritance. A sperm cell only contributes its nuclear DNA but not the mitochondrial DNA during fertilization. The mitochondrial genome of an offspring is determined entirely by female mitochondrial DNA present in the egg and is therefore exclusively maternally inherited. Therefore, no mitochondrial disease may be transmitted from males to any of his offspring.

Mitochondrial Disorders
mtDNA is not highly conserved and has a significantly higher mutation rate. The base substitution rate is pretty high than in nuclear genome. Deletions and other rearrangements are also common. Many mtDNA mutations are expressed as abnormal phenotypes at the cellular and organism level.
The mtDNA is more prone to mutations because of proximity to free-radicals generated during oxidative phosphorylation and because of absence of a DNA integrity maintenance system as it exists for nuclear DNA.

In humans, many genetic conditions are related to changes in particular mitochondrial genes and are called mitochondrial cytopathies. Some conditions that are associated with the changes in mitochondrial DNA include, but are not limited to:

Cancers: Somatic mutations in mtDNA have been reported in some forms of cancer, including breast, colon, stomach, liver, and kidney tumors.

Cyclic vomiting syndrome: Certain changes in mtDNA related to cyclic vomiting syndrome which is associated with recurrent episodes of nausea, vomiting, and lethargy that may last from few hours to few days!

Leber hereditary optic neuropathy (LHON): It is characterized by bilateral, painless, subacute visual failure that develops during young adult life. Many mitochondrial genes have been identified with mutations in people with Leber hereditary optic neuropathy.

Neuropathy, ataxia, and retinitis pigmentosa (NARP): Many mutated mitochondrial genes have been found in people with neuropathy, ataxia, and retinitis pigmentosa (NARP) which features weakness of the trunk muscles, wobbliness, retinal disease, seizures and developmental delay. There is a mutation in an enzyme called complex V which is involved in oxidative phosphorylation i.e. generation of ATPs!