ONLINE BRIEFING –  Thursday May 17, 12.30pm AEST

In the first study of its kind in Australasia, scientists have used 27 natural climate records to create the first large-scale temperature reconstruction for the region, over the past 1000 years.

 The study, led by researchers at the University of Melbourne, used a range of natural indicators including tree rings, corals and ice cores to reconstruct Australasian temperature over the past 1000 years. The results show that there are no other warm periods in the last 1000 years that match the warming experienced in Australasia since 1950.

Comparison with climate model data reveals that the warming cannot be explained by natural factors alone, suggesting a strong influence of human-caused climate change in the region.

This study gives an insight into the next IPCC report, as it will form the Australasian region’s contribution to the chapter on past climate of the last 1000 years. The research is published in the Journal of Climate today:

UniMelb media release

Paper

Briefing powerpoint presentation

The briefing will discuss the following issues:

• Natural variability in Australasia over last 1000 year

• How does modern climate change compare to the ‘little ice age’ and ‘medieval warm period

• How unusual is recent climate warming?

 SPEAKERS:

• Dr Joelle Gergis is an ARC Research Fellow at the School of Earth Sciences at the University of Melbourne. She is leader of the Past Global Changes (PAGES) working group on Australasian climate of the past 2000 years (Aus2K) and lead author of the study

•  Professor David Karoly is a Professor of Climate Science and leader of the Climate Change theme in the Melbourne Sustainable Society Institute at the University of Melbourne 

• Dr Steven Phipps is a research fellow at the Climate Change Research Centre and ARC Centre of Excellence for Climate System Science at the University of New South Wales

 BRIEFING DETAILS:

DATE: Thu 17 May 2012

START TIME: 12.30pm AEST

DURATION: 30 min

VENUE: Online

For further information and instructions for logging into the event, please contact us on 08 7120 8666 or by email.

——–

UK researchers report that inducing labour at more than 37 weeks of gestation reduces the rate of stillbirth or dying in the first month of a baby’s life, without increasing the rate of caesareans. However, inducing labour increased the number of babies admitted to neonatal intensive care compared with standard labour management. The researchers analysed pregnancies in more than one million women from 1981 until 2007.

One of the authors, Dr Sarah Stock from the University of Edinburgh, is currently on a Maternal-Fetal Medicine Fellowship at Perth’s King Edward Memorial Hospital and with the University of Western Australia’s School of Women’s and Infants’ Health.

Feel free to use these quotes in your stories. Any further comments will be posted here. The research material is available in the registered area. If you would like to speak to an expert, please don’t hesitate to contact us on (08) 7120 8666 or by email.

———–

Professor Mary-Ann Davey is a Senior Research Fellow at Mother & Child Health Research at La Trobe University, Melbourne. Prof Davey is independent of the study

“This study looks at routinely-collected records for over one million births of full-term, singleton babies in Scotland between 1981 and 2007. They compared a number of outcomes between the women whose labour was induced at each week of gestation between 37 and 41 weeks with those women whose labour was not induced.

They found that babies born after induced labours were less likely to be stillborn or to die in the first month of life, and that unassisted vaginal birth was no less likely with induced labours. However babies were more likely to be admitted to neonatal intensive care and special care nurseries following induced labour, and their mothers were more likely to experience two adverse outcomes: ruptured uterus and difficulty delivering the baby’s shoulders.

Some apparent problems with this study include:

• Women were excluded from the induced group if they had specified complications of pregnancy recorded, but women were not excluded from the comparison group if they had these conditions recorded. This means that the induced group is likely to be a healthier group of mothers than those not induced, so would be expected to have fewer adverse outcomes and fewer operative births.
• Babies whose labour was not induced were more likely to be poorly grown than those who were induced, placing them at greater risk of death, and also of caesarean birth.
• It is not clear when babies in the comparison group died (assumptions were made), so it is not certain that induction of labour at any particular time could have prevented their death.

Studying elective induction of labour is very difficult to do well. Even large randomised controlled trials in the area have been seriously flawed. There remains considerable work to do on the impact of elective induction of labour.”

 Prof Davey is unavailable this evening but will be able to do interviews tomorrow.

 ———–

Professor Jenny Gamble is Professor of Midwifery and Maternity and Family Unit Leader at the Research Centre for Clinical and Community Practice Innovation at Griffith University. Prof Gamble is independent of the study

“This study compares medically managed birth (elective induction) with expectant management. Usual care for women in the expectant management (comparator) group was likely to involve labour care by people the woman had not met before and with no assurance of one-on-one care in active labour. On the other hand, women undergoing elective induction may have had increased observation and attendance by midwives and/or doctors and this may have affected the outcome. There is significant evidence that continuity of care by a known midwife improves a range of outcomes for women and their babies, and it may well be that healthy pregnant women trying to birth in medicalised environments are at greater risk than women under closer medical management such as during induction of labour. Research into the use of medical interventions on childbearing women should ensure that the comparator group is receiving evidence-based care.

Women with medical indications for induction were excluded from the elective induction of labour group but not excluded from the comparator group (expectant management). There may well have been significant numbers of women in the comparator group with medical indications for induction but not induced (e.g. hypertension or previous still birth) and this may have inflated perinatal mortality in the comparator group. Similarly, women with prelabour rupture of membranes were excluded from the elective induction group but not the comparator (expectant management) group, yet prelabour rupture of membranes, particular when this is prolonged, is associated with an increased rate of complications for the fetus and newborn.

Admission to neonatal nursery was increased in association with elective induction of labour at all gestations and is of serious concern. Despite this, the extent of newborn health concerns was not documented. We do not know about the babies’ condition at birth (Apgar score), reason for admission to neonatal nursery, length of neonatal nursery stay, impact on breastfeeding, or associated costs. No data is provided on short, medium or long-term neonatal morbidity of elective induction at term in healthy women.”

 ———–

 *Outcomes of elective induction of labour compared with expectant management: population based study, Stock et al., BMJ, 11 May 2012

Research from the US shows exposure of pregnant rhesus monkeys to Bisphenol A (BPA) altered the developing mammary glands of their offspring. BPA is used in the manufacturing of various plastics and resins for food packaging and consumer products. BPA can act as an endocrine disruptor (a chemical that can interfere with the balance of hormones in the body); specifically, BPA has been found to mimic oestrogen (in animal models), with implications for development and reproduction. 

Feel free to use these quotes in your stories.  If you would like a copy of the research or to speak to an expert, please don’t hesitate to contact us on (08) 7120 8666 or by email.

———–

Dr Ian Musgrave is a senior lecturer in the Discipline of Pharmacology at the University of Adelaide

Is this research and its findings of concern to the human population?

“No, doses used and plasma concentrations reached do not represent most human exposure (see next section). The only significant finding was that the number of terminal buds in breast tissue were increased. This is of doubtful relevance to cancer. No other aspect of breast tissue structure at the gross or microscopic level was changed. “

Is the dosage used in the report similar to that of the regular person’s exposure to Bisphenol A?

“No, the dosage used was 8 times higher than the upper limit of permitted human exposures. It was also administered as a single, large dose which would have produced a much larger concentration in the blood than was seen when the plasma levels were measured 4 hours later. The serum level of total BPA measured at this time were around 50 times higher than is seen in several human studies, but as this plasma level was measured several hours after dosing, the actual exposures would be much higher.” 

Should this be a warning of the dangers of Bisphenol A exposure during pregnancy or infant developmental stages?

“In long term studies with rats at these high levels of exposure, no adverse effects have been seen.” 

Is there a way to lower ones exposure to the Bisphenol A, considering its ubiquity in the modern world?

“The best way is to consume less processed food. This reduces BPA intake, and also limits salt, sugar and fat intake which also has important health benefits.”

 ———–

 Comments from the UK SMC:

Professor Warren Foster, Department of Obstetrics & Gynecology, McMaster University, said:

 “The paper by Tharp et al., 2012 examined the effect of developmental exposure to Bisphenol A (400 ug/kg BW) given from gestational day 100 to term in rhesus monkeys. At birth the mammary glands were removed and examined either by whole mount or histomorphometry and immunohistochemistry for estrogen receptors. The paper has a number of strengths which include the use of a non-human primate model that more closely reflects human development and physiology. In addition, the animals were exposed via an oral route to the test compound and the methods of analysis are appropriate for the stated objectives.

 “There are several weaknesses with this paper which include but are not limited to the small sample size. It is appreciated that non-human primate studies are expensive and difficult to run, yet four and five animals/group is not robust and it is difficult to extrapolate the findings to the larger population. Furthermore, the authors state that their dosing paradigm resulted in blood concentrations of free BPA that are representative of the human population as summarized in the Vandenberg and colleagues review paper.  However, the exposure to BPA is not representative of how humans are exposed. Specifically, the monkeys received a single high dose exposure which, at the time samples were collected, produced a circulating concentration that was representative of human serum concentrations. Note that the serum concentrations in human studies are in the range quoted in this study in small biomonitoring studies, whereas more recent larger studies show lower median concentrations. Moreover, humans are primarily exposed to BPA through the diet to low concentrations of BPA. Of note a recent pharmcokinetic study conducted by Teegaurden and colleagues shows that people consuming meals with relatively high concentrations of BPA did not result in detectable concentrations of BPA in their circulation, while conjugated BPA was measured in the urine. Hence, a large bolus of BPA administered once during the day can result in very high circulating concentrations of free BPA in the serum that fall through the concentration reported in biomonitoring studies but may not necessarily be reflective of how people and tissues are exposed. Other minor criticisms may arise from the use of a single dose and the absence of a positive control group for comparison. Finally, the results demonstrate premature development of the mammary gland but do not demonstrate any pre-cancerous lesions.

“Overall, this is a scientifically sound paper that extends the findings in rodents to the non-human primate. The results do not however suggest that BPA is a carcinogen or that it is implicated in breast cancer. Furthermore, the dosing paradigm is not representative of human exposure which make generalization of the study results to humans difficult.”

———- 

Professor Richard Sharpe, MRC Centre for Reproductive Health, Edinburgh University, said:

“This preliminary study shows that fetal exposure of rhesus monkeys to high levels of bisphenol A (a weakly oestrogenic chemical) may result in an increase in terminal end buds in mammary glands at birth (the only significant finding). It is unlikely the effects described have any health implications for humans, for two reasons.

 “First, the exposure levels of BPA used in this study are 400- to 4000- times higher than exposure of the normal human population. Levels of unconjugated (biologically active) bisphenol A in blood in humans are so low they cannot be measured; this is probably because ingested bisphenol A is rapidly inactivated during absorption from the gut.

 “Second, at birth in humans breast tissue is enlarged (boys as well as girls) because of exposure to the extremely high pregnancy levels of oestradiol. Additional exposure to minimal amounts of bisphenol A (more than 1000 times less potent than oestradiol) is unlikely to add significantly to this.

 “Similar effects on mammary terminal end buds have been shown in laboratory rats exposed to bisphenol A, but again at exposure levels many times higher than in humans (as in the monkeys). However, even then no adverse long-term effects (eg mammary cancer) from exposure to bisphenol A alone have been shown to result.

 “Statistical note:

This is an extremely small study (N=4, 5) and terminal end bud number varied hugely in controls and overlapped with values for bisphenol A-exposed animals. This could mean the present findings are due entirely to chance.”

 * ‘Bisphenol A alters the development of the rhesus monkey mammary gland’ by Tharp et al. www.pnas.org/cgi/doi/10.1073/pnas.1120488109

———–

Researchers from the University of Adelaide have compared the risk of major birth defects for each of the reproductive therapies commonly available internationally, including IVF. Below experts respond.

Feel free to use these quotes in your stories.  Any further comments will be sent out and posted here. To speak to an expert, please don’t hesitate to contact us on (08) 7120 8666 or by email. The research paper is available on the registered area of this site.

———–

Professor Peter Illingworth is Medical Director at IVF Australia and an Associate Professor with the University of Sydney

“This paper confirms the previously widely reported association between babies being conceived through assisted reproduction technologies (ART) and having a slightly higher risk of congenital anomalies.

These findings are consistent with previously widely reported data in this area. What is new about this paper is that Professor Davies has, for the first time, looked at other women in similar situations.

The big question underlying the association between assisted reproduction and congenital anomalies is whether this is due to the laboratory process itself, or whether it’s a reflection of the fact that people who have to use ART to have their family already have pre-existing damage to their eggs and sperm that puts them at higher risk of having children with congenital anomalies. 

Professor Davies’ findings suggest the later explanation. He has, for the first time, looked at the siblings who have been conceived normally of children who have been conceived from ART. He has also looked at women who have presented to antenatal clinics with a past history of infertility but who have not had ART. Both of these groups show a very similar effect, with a higher risk of congenital anomalies, as do the children who have been conceived using ART. This is a new finding.

The other interesting feature about his results is the fact that, when he separates the two types of ART into IVF and intra-cytoplasm sperm injection (ICSI), his findings are that IVF children do not have a higher risk of congenital anomalies and that the risk is limited to children who have been conceived using ICSI. This is contrary to other findings in large studies in Europe. The explanation for this is not at all clear. It may well be that the sort of families who have to use ICSI have extreme sperm damage, and this may be the explanation as to why there is a higher rate of congenital anomalies in this group.

I think this is a very important paper; it’s one that we’ve needed for a long time. I think Professor Davies should be congratulated on his work.”

———–

The following comment was obtained by our colleagues at the UK Science Media Centre:

Dr Allan Pacey, fertility expert at the University of Sheffield and Chairman of the British Fertility Society, said:

“This is an interesting paper which analyses the register of birth defects in South Australia with the data from clinics providing infertility treatments such as IVF and ICSI. This is with the aim of trying to find any links between the two, a common approach in this kind of work requiring large numbers of patients to make sure any statistical associations are robust.

 “Several links are found by the authors, but these largely confirm what is already known and suggest that whilst babies born from IVF are as healthy as their naturally conceived counterparts, there is still some residual risk to babies born through ICSI that currently cannot be explained. An important point to make is that we know that babies conceived naturally to couples previously diagnosed with infertility are also at slightly higher risk which suggests that it may be something to do with the ‘infertility’ rather than the ‘technology’ used to conceive them.

 “Couples undergoing assisted conception are understandably concerned about the potential health of any babies born and studies like this are enormously helpful in giving them accurate information and helping to put the risk into context. It should be stressed that the vast majority of babies born are healthy and the actual risks of any problems being detected are small.”

 ———–

 *Reproductive Technologies and the Risk of Birth Defects, Davies et al., New England Journal of Medicine, 10.1056/nejmoa1008095, 2012

Researchers have shown that the H5N1 ‘bird flu’ virus, which is highly dangerous but so far not easily spread between mammals ( including people), could easily acquire this ability. The researchers crossed the H5N1 strain with the pandemic H1N1 strain which swept the globe in 2009 and showed that the resulting virus could easily pass between ferrets. While ferrets are a long way from humans, it suggests that similar viruses with pandemic potential in humans may emerge. The publication of this paper follows a long debate about the potential biosecurity risks from publishing this research.

 ————-

Canadian SMC comments:

Dr. Udo Schuklenk Professor of Philosophy, Queens University More on Udo Schuklenk “This comes back to an old debate in biotechnology on the ethics of biochemical warfare research. There are so many rogue regimes, Iran, North Korea, and this work is also undertaken by Western governments,although some of it may be defensive in nature.  The question is, should you continue, should you publish your research even if that would help terrorists to get their hands easier on such weapons than they would be able to otherwise. The response is that you can’t keep the lid on anyway, this information will get out and it will be used anyway, so it should be published because then more people can work on defensive measures. The assumption is that eventually, information will get out – you can’t keep the lid on it. A mailing list, a computer that gets lost, the possibilities are endless and so, at one point it will be in the open. We are probably better off controlling how and when it happens. You plan for the worst case scenario, and people will be prepared. There are no contained channels of knowledge, that’s a fiction. If you send it to WHO, for instance, within two seconds, it’s all over the world, courtesy of the internet. You can’t control these things. Scientists go to conferences, talk to colleagues, email colleagues, their emails could be hacked, you can go on forever thinking about not terribly unlikely accidental dissemination scenarios.

Do you think that restricting the publication of such research would discourage researchers from working in the field? I doubt it. if you put a lot of funding on the table on the condition that you can’t publish your research but you are paid well for the rest of their life, and you can undertake cutting edge research in lab facilities that are second to none … Think of scientists working for a company, signing a non-disclosure agreement. They do not quit in their hundreds because they can’t always publish the results of their research. It’s not true that all academics go into research to publish and become famous. Some do, but many don’t. I think they should publish, I don’t think they have a choice.”

————

Dr. Andrew Potter Director, Vaccine and Infectious Disease Organization, University of Saskatchewan. More on Andrew Potter “The issue that was put forward was that if this work fell into the wrong hands, would be of benefit to people who wanted to do harm. So, does one then go ahead and publish? Or do you keep it a secret? There’s been a lot of debate. I think it’s horrendously dangerous to keep this type of work secret. These things do happen in nature, that’s how you get the deadly pandemics. They do happen. If we don’t do the research and publish the research, we will forever be in the situation of reacting to pandemics instead of being proactive. From my perspective it’s valuable to have this information out there, so we can start planning. That way, if and when a pandemic hits, we can mobilize something that exists instead of having to develop something that doesn’t yet exist. . We make the assumption that people who want to use this information for harm are pretty stupid and would have to read this paper to get this information and use it. One has to give the other side the benefit of the doubt that they have already been looking at this and other agents, and if they had a desire to develop it, the chances are they could. I worry more about someone getting a vial of smallpox for terrorism purposes. People have been preaching over the last decade to watch out for this event; i.e. a highly transmissible H5N1 pandemic. From a Canadian perspective, it’s good to have debates, and that has led to new regulations on this type of work. They bumped [research on this virus] up into Level 4 – so that any highly transmissible highly pathogenic influenza virus can only be studied in a Level 4 containment lab such as the federal lab in Winnipeg. In Canada, that’s only one lab I know of, [the Canadian Science Centre for Human and Animal Health], in Winnipeg. But you’re not going to generate knowledge if you just sit and wait.

If this research wasn’t made public, how would it have been used? If one treats it as a trade secret and communicates it selectively, is that really private? The information is useful to governments, people who regulate this type of thing, as well as groups such as the WHO.  Therefore, one could gain the benefit of the information without it going public through selective release.

What are the benefits of making it public? A couple of things. As with any significant experiment, other people try and reproduce it to make sure its really true. You need that duplication. It also forms a basis where one can proactively develop control strategies. The paper describes some great research and it’s great these people carried it out and it is well worth publishing. The public needs to take a step back and look where the real risk is, and approach it from a risk based perspective relative to other threats.”

————

Comments from the UK Science Media Centre

Dr John McCauley, Director of the WHO Collaborating Centre for Influenza at the MRC National Institute for Medical Research said:

“While we understand the concerns raised about the publication of this research, we are very pleased that it is now available. The Medical Research Council’s policy on Bioterrorism and Medical Research clearly outlines the considerations which have to be made when making funding decisions about work of this nature. The study published in Nature is an important piece of the puzzle at the WHO Collaborating Centre for Influenza at the MRC National Institute for Medical Research, who are trying to put together a clearer picture of how these viruses might spread from human to human and understand the evolution of these viruses that have proved so devastating for birds and could yet do so for humans.”

 The policy can be found here: http://www.mrc.ac.uk/Utilities/Documentrecord/index.htm?d=MRC002538

————

Prof Wendy Barclay Chair in Influenza Virology, Imperial College London “This is a significant piece of research. The work is elegantly performed and contributes new knowledge in two ways: “First it describes the use of randomly generating influenza mutants in the lab and phenotypically selecting them, in a way that speeds up what nature is doing. This allowed the identification of novel mutations that altered the H5 HA receptor binding specificity. “However, what is interesting is that although this approach was good enough to pull out the receptor binding changes it was designed to find, it did not in the end solve the mystery of transmissibility because there is more to it than that: in other words we are always limited by our lack of knowledge when designing the best screens. “In the end the approach gave the helping hand that allowed the virus to replicate well enough in the right place in the ferret to then select, by a more traditional forward genetic approach, mutations that affect the stability of the HA protein. This is a new finding. “The second piece of novel information in the paper is that HA needs to be stable to be transmissible through the air between mammals. With hindsight it makes perfect sense that the virus has to be very stable to survive in acidic conditions whilst it is outside the cell, others have also pointed out before that the nose can be a relatively acidic environment. “I think what we can conclude concerning surveillance efforts is that sequencing on its own might never be enough – the virus can make changes in amino acids of HA (and probably other genes) that affect transmissibility in ways that we might not have previously imagined. “We know now more about how an avian virus has to change to become transmissible, but we need to bear in mind that the mutations we pick up during surveillance in the wild need to not only be mapped onto the three-dimensional structure of the HA protein, but also understood in terms of their effects on behaviour of the virus in order to know if they are to be taken seriously.”

[*Experimental adaptation of an influenza H5 HA confers respiratory droplet transmission to a reassortant H5 HA/H1N1 virus in ferrets. M. Imai et al. Nature http://dx.doi.org/10.1038/ nature10831 (2012)]