Fasting mothers raise potential risk for unborn babies
AS RAMADAN begins this week, pregnant women deciding whether to take part in the customary fast may wish to consider the effect on their babies.
So says Nick Ashton at the University of Southampton, UK, and colleagues at King Saud University in Riyadh, Saudi Arabia. They analysed records of 7000 babies born in a Saudi hospital over a four-year period, and worked out during which trimester, if any, of their mother's pregnancy Ramadan fell. Surveys indicate that over 90 per cent of pregnant Muslim women fast.
While babies' birth weights were similar in fasting and non-fasting Saudi women, the placentas of women who had fasted during the second or third trimester were 3 per cent lighter than average when the child was a boy and 1.5 per cent lighter for girls (Placenta, DOI: 10.1016/j.placenta.2010.04.010).
Children born with placentas that are smaller than average are known to have an increased risk of cardiovascular disease later in life, though it is too early to advise pregnant women whether to fast, Ashton says. "Birth weight isn't affected, which is good, but we need to see whether a small placenta affects the risk of cardiovascular disease in these children in the long term."
So says Nick Ashton at the University of Southampton, UK, and colleagues at King Saud University in Riyadh, Saudi Arabia. They analysed records of 7000 babies born in a Saudi hospital over a four-year period, and worked out during which trimester, if any, of their mother's pregnancy Ramadan fell. Surveys indicate that over 90 per cent of pregnant Muslim women fast.
While babies' birth weights were similar in fasting and non-fasting Saudi women, the placentas of women who had fasted during the second or third trimester were 3 per cent lighter than average when the child was a boy and 1.5 per cent lighter for girls (Placenta, DOI: 10.1016/j.placenta.2010.04.010).
Children born with placentas that are smaller than average are known to have an increased risk of cardiovascular disease later in life, though it is too early to advise pregnant women whether to fast, Ashton says. "Birth weight isn't affected, which is good, but we need to see whether a small placenta affects the risk of cardiovascular disease in these children in the long term."
MRI scans could diagnose autism
Ten minutes in a brain scanner could be all it takes to diagnose autism. So says Christine Ecker at the Institute of Psychiatry, UK, who has developed software that identifies the anatomical signatures of the condition.
Ecker's team carried out MRI scans on the brains of 20 adult males with autism, 20 with attention-deficit disorder and 20 healthy controls. They used a machine-learning tool called a support vector machine (SVM) – which analyses data and identifies patterns – to identify key differences between the groups, such as in the cortical folding and curvature of the brain.
The SVM was then used to build a model to predict whether brain scans fall into the autistic or control group. When the original scans were fed into this model, it diagnosed autism with a 90 per cent success rate.
Current diagnosis tools are based on time-consuming and potentially stressful behavioural tests and interviews. Ecker now plans to test her model on children, for whom she predicts more accurate results "because the differences in anatomy between the healthy and autistic brain are more prominent in childhood".
"The authors have been very careful to use this tool on a very specific group, and are not claiming that it will work on the whole spectrum of autism," says Uta Frith at University College London. "This is just the beginning, a proof of concept. It would be necessary to try it out on a new group and see whether the same results would be obtained."
She adds that studying brain anatomy alone is not enough: "We need to understand how the differences in anatomy are somehow bound up with functional differences in mental life, in how people think and feel."
Ecker's team carried out MRI scans on the brains of 20 adult males with autism, 20 with attention-deficit disorder and 20 healthy controls. They used a machine-learning tool called a support vector machine (SVM) – which analyses data and identifies patterns – to identify key differences between the groups, such as in the cortical folding and curvature of the brain.
The SVM was then used to build a model to predict whether brain scans fall into the autistic or control group. When the original scans were fed into this model, it diagnosed autism with a 90 per cent success rate.
Current diagnosis tools are based on time-consuming and potentially stressful behavioural tests and interviews. Ecker now plans to test her model on children, for whom she predicts more accurate results "because the differences in anatomy between the healthy and autistic brain are more prominent in childhood".
"The authors have been very careful to use this tool on a very specific group, and are not claiming that it will work on the whole spectrum of autism," says Uta Frith at University College London. "This is just the beginning, a proof of concept. It would be necessary to try it out on a new group and see whether the same results would be obtained."
She adds that studying brain anatomy alone is not enough: "We need to understand how the differences in anatomy are somehow bound up with functional differences in mental life, in how people think and feel."
Early puberty in girls doubles in a decade
Twice as many white girls in the US reach puberty aged 7 as a decade ago. No one is sure why this should be the case, but obesity and exposure to chemicals that mimic the female hormone oestrogen are the prime suspects.
The figures come from a study of 1200 girls in three US cities. Of the girls studied, 10.4 per cent of white 7-year-olds had breast development consistent with the onset of puberty, compared to 5 per cent in a 1997 study.
Earlier studies had identified early puberty mainly in black girls.
Marcia Herman-Giddens of the University of North Carolina at Chapel Hill, who led the 1997 study, expressed shock at the increases.
"To find the girls are starting breast development earlier and earlier is extremely concerning," she says. "To have that much change in such a short time, it has to be the environment."
It appears that the proportion of black 8-year-olds entering puberty has dropped from 48 per cent in 1997 to 43 per cent today. Frank Biro of the Cincinnati Children's Hospital Medical Center in Ohio, head of the new study, suggests this might be a sign that the numbers of black girls experiencing early puberty may finally be levelling off, while the percentage of white girls affected is still rising.
"Part of it is the increase in overweight and obese girls," says Biro. Hormones released by the extra fat cells could play a role. His team is also checking blood and urine samples for chemicals that mimic oestrogen, from plastics in the environment, for example, to soya in the diet.
The figures come from a study of 1200 girls in three US cities. Of the girls studied, 10.4 per cent of white 7-year-olds had breast development consistent with the onset of puberty, compared to 5 per cent in a 1997 study.
Earlier studies had identified early puberty mainly in black girls.
Marcia Herman-Giddens of the University of North Carolina at Chapel Hill, who led the 1997 study, expressed shock at the increases.
"To find the girls are starting breast development earlier and earlier is extremely concerning," she says. "To have that much change in such a short time, it has to be the environment."
It appears that the proportion of black 8-year-olds entering puberty has dropped from 48 per cent in 1997 to 43 per cent today. Frank Biro of the Cincinnati Children's Hospital Medical Center in Ohio, head of the new study, suggests this might be a sign that the numbers of black girls experiencing early puberty may finally be levelling off, while the percentage of white girls affected is still rising.
"Part of it is the increase in overweight and obese girls," says Biro. Hormones released by the extra fat cells could play a role. His team is also checking blood and urine samples for chemicals that mimic oestrogen, from plastics in the environment, for example, to soya in the diet.
Prompting hearts to make their own beating muscle
Beating heart muscle cells have for the first time been made directly from other heart cells. The breakthrough may enable damaged heart muscle to be repaired by converting the structural cells called fibroblasts into the cardiomyocytes that make the heart beat.
The route from fibroblasts to cardiomyocytes is so direct that no transitory stem cellsMovie Camera need to be formed in the process, avoiding the extra step by which many other researchers are trying to create heart cells from patients' own cells, or from human embryonic stem cells.
"Other teams, including ours, have spent significant effort making cardiomyoctes from stem cells for regenerative purposes," says Deepak Srivastava of the Gladstone Institute of Cardiovascular Disease in San Francisco.
The route from fibroblasts to cardiomyocytes is so direct that no transitory stem cellsMovie Camera need to be formed in the process, avoiding the extra step by which many other researchers are trying to create heart cells from patients' own cells, or from human embryonic stem cells.
"Other teams, including ours, have spent significant effort making cardiomyoctes from stem cells for regenerative purposes," says Deepak Srivastava of the Gladstone Institute of Cardiovascular Disease in San Francisco.
Change of heart
Now Srivastava and his team have created mouse cardiomyocytes by exposing mouse fibroblasts to three transcription factor proteins called Gata4, Mef2c and Tbx5 that activate genes needed for the formation of embryonic heart tissue. "The fibroblasts started to convert within a few days and continued to make the transition to cardiomyocytes over several weeks, beating at about one month," Srivastava says.
The team also transplanted treated fibroblasts into the hearts of live mice, where they developed into cardiomyocytes.
Next, Srivastava's team will see if the process works on human fibroblasts. They will also hunt for ways to morph fibroblasts without having to first infect them with a virus – which is how the transcription factors were transported to the mouse fibroblasts.
The team also transplanted treated fibroblasts into the hearts of live mice, where they developed into cardiomyocytes.
Next, Srivastava's team will see if the process works on human fibroblasts. They will also hunt for ways to morph fibroblasts without having to first infect them with a virus – which is how the transcription factors were transported to the mouse fibroblasts.
