Men suffering from from non-obstructive azoospermia (NOA), meaning they have undetectable levels of sperm in their semen, which is not caused by an obstruction in their reproductive system, have long been considered poor candidates for IVF (in vitro fertilisation). However new research published in the online journal of Reproductive Biology and Endocrinology has reported that NOA sufferers could be just as capable of producing viable embryos as other men.
Approximately one per cent of the male population and 10 per cent of men seeking fertility evaluation have testicular failure. Previous research conducted by Belgian scientists reported lower pregnancy rates than normal (approximately 20 per cent) when using sperm from NOA patients. It has also been thought that sperm isolated from NOA patients, while able to produce embryos, is less capable of producing live births and that the incidence of genetic mutations may be higher resulting in congenitial deffects. However, new research contradicts this and gives hope that men with NOA can be just as likely to father a child.
Nina Desai and her team at the Cleveland Clinic Foundation analysed 156 ICSI (intracytoplasmic sperm injection) cycles which used sperm taken from the testes of 44 men suffering from obstructive azoospermia (OA) and 17 men diagnosed with NOA. For their study they assessed embryonic development, implantation, pregnancy and live birth rates. They found on all counts that there were no significant differences between the groups.
Desai and her team analysed the ability for the pateranl sperm to iniate genomic activation, this is when the genome of the embryo divides and begins to arrange itself. They way to morphologically measure this is to observe the degree of cell to cell aderence as the embryo cells divide, if there is genomic activation it is thought that by the eight-cell stage there will be an increase in cell-cell adherence. The anaysis found no differences between the sperm groups suggesting that the genome activation is independent of sperm origin and type of azoospermia. They also noted that there were no cogenital abnormalities in the 115 healthy births.
Tuesday, January 19, 2010
Monday, January 18, 2010
Key to long life is having two mothers but no father!
Mice produced in the laboratory from two biological mothers and without a father have been found to live significantly longer than normal mice bred from a mother and a father. These findings indicate that genetic traits inherited from the father but not the mother may play an important role in ageing and longevity.
Researchers from Saga University and Tokyo University of Agriculture, Japan, took DNA (deoxyribonucleic acid) from eggs of one day-old mice and genetically modified it so that it would behave like sperm. They then used it to fertilise eggs from adult mice, thereby producing offspring with two mothers, dubbed bi-maternal mice. Control mice were bred that were genetically identical to the bi-maternal mice except that they had been conceived conventionally using genetic material from a sperm and an egg.
Professor Tomohiro Kono, who led the study, explained the researchers' goals: 'We have known for some time that women tend to live longer than men in almost all countries worldwide, and that these sex-related differences in longevity also occur in many other mammalian species... The study may give an answer to the fundamental questions: that is, whether longevity in mammals is controlled by the [genes] of only one or both parents, and just maybe, why women are at an advantage over men with regard to the lifespan.'
Reporting in the journal Human Reproduction, the researchers compared the lifespans of 13 bi-maternal mice with those of 13 control mice. On average, the bi-maternal mice lived for 841.5 days - 186 days longer than the control mice, which averaged 655.5 days. The researchers also found that the bi-maternal mice were significantly smaller and lighter than the control mice. There were also signs that the bi-maternal mice had better immune systems than the control mice, as they had higher numbers of eosinophils (a type of white blood cell that play an important role in protecting mammals against parasites and infections) in their blood.
The researchers believe that the effects they observed may result from a genetic process called 'imprinting' whereby the activity of a gene depends on whether it is inherited from the mother or the father. They suggest that a gene called Rasgrf1, found on chromosome 9, may be responsible for the increased lifespan and smaller weight of the bi-maternal mice.
Rasgrf1 is an imprinted gene that is always turned on when it is inherited from the father and always turned off when it is inherited from the mother. The bi-maternal mice had two inactive Rasgrf1 genes as they were both inherited from female mice instead of having the usual one active Rasgrf1 gene inherited from a father and one inactive Rasgrf1 gene inherited from a mother. However, Professor Kono emphasised: 'it's not clear whether Rasgrf1 is definitively associated with mouse longevity, but it is one of the strong candidates... we cannot eliminate the possibility that other, unknown genes that rely on their paternal inheritance to function normally may be responsible.'
Professor Kay-Tee Khaw, an expert in ageing at Cambridge University, commented to the BBC: 'These are interesting findings but I think any sex differences in longevity - which in humans have changed over time and differ in different environments - may have more complex explanations than any single gene'.
Sunday, January 17, 2010
Finally, the true story....
If you have heard this one before then it is still worth a second read !!!
Some time ago, President Clinton was hosting a state dinner when, at the last minute, his regular cook fell ill, and they had to get a replacement on short notice.
The fellow arrived and turned out to be a very grubby-looking man named Jon. The President voiced his concerns to his Chief of Staff but was told that this was the best they could do on such short notice.
Just before the meal, the President noticed the cook sticking his finger in the soup to taste it and again complained to the Chief of Staff, but he was told that this man was supposed to be a very good chef. The meal went okay, but the President was sure that the soup tasted a little funny. By the time dessert came, he was starting to have stomach cramps and nausea.
It was getting worse and worse until finally the President had to excuse himself from the dinner to look for the bathroom. Passingthrough the kitchen, he caught sight of the cook, Jon, scratching his rear end, which made him feel even worse.
By now, the President was desperately ill with violent cramps and was so disorientated that he couldn't remember which door led to the bathroom. He was on the verge of passing out from the pain when he finally found a door that opened. As he unzipped his trousers and ran in, he realized to his horror that he had stumbled into the office of Ms.Monica Lewinsky with his trousers around his knees.
As he was just about to pass out, she bent over him and heard the President whisper in a barely audible voice, 'Sack my cook.'
And that is how the whole misunderstanding occurred...
Saturday, January 16, 2010
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