South Australians don’t see heatwaves as serious events and warnings do little more than ‘trigger’ common-sense behaviours like turning on the air-conditioner, new research from the University of Adelaide shows.
The research, conducted by the University’s School of Public Health, found that South Australians do not perceive heatwaves as high risk events, an attitude compounded by TV news items, which tend to show images of people enjoying the beach during heatwaves, rather than heatwaves as potentially broadly dangerous events.
Lead author Dr. Scott Hanson-Easey says news stories that include people swimming at the beach lead the majority to believe that only vulnerable people need to take care.
“For the most part, our findings showed messaging was framed in accord with media norms and values that rendered information as infotainment,” Dr. Hanson-Easey says.
“Our data suggest that TV-news reporting is most likely contributing to heatwave risk being normalised and information being met with scepticism and irritation.”
The research, an Australian first, will help guide state emergency services and other government agencies to construct more appropriate messages as current information is not reaching the right people in the right way.
“Although age and poor health has been used as key criterions to identify vulnerability and segment target audiences, we suggest that this criterion is too blunt and may be missing households who struggle with multiple and interlaced social vulnerabilities, including poor quality housing, living in ‘hot spot’ suburbs (urban heat islands caused by lack of vegetation), low SES, and health problems,” says Dr. Hanson-Easey.
“Our findings strongly suggest that, for a majority of the public, message fatigue is not being perceived in relation to heatwave warnings and messages. Heatwave information is construed as redundant – as ‘already known’ knowledge that is not adding anything new to how individuals understand heatwaves and their adaptation options.
“Communication efforts will, if they are to remain relevant, need to adjust messaging to accord with this belief and the lived experiences of the public in a capricious social, economic and environmental climate.”
Reduced growth hormone receptor signalling improves insulin signalling within the body.
University of Queensland researchers have discovered a hidden metabolic advantage that prevents people with a specific type of dwarfism from developing type 2 diabetes or cancer.
UQ Diamantina Institute researcher Dr. Yash Chhabra said the findings could pave the way for new diabetes treatments for all.
“We set out to understand why, unlike most people, people with Laron dwarfism don’t develop diabetes despite being obese,” Dr. Chhabra said.
“People with Laron dwarfism aren’t sensitive to growth hormone due to a defective growth hormone receptor in their cells.
“Growth hormone is responsible for regulating height, metabolism and obesity.
“Having defective receptors also means Laron dwarfs remain highly sensitive to insulin.”
Emeritus Professor Michael Waters said normally when a person became obese, their sensitivity to insulin decreased and they eventually developed type 2 diabetes.
“Our study clarifies an issue that has been unresolved for 50 years,” Professor Waters said.
“We discovered that a signalling molecule activated by the growth hormone receptors, called STAT5, was responsible for regulating this insulin sensitivity.
“This switching off of the STAT5 activation improved prevented insulin resistance by improving insulin signalling.
“This increased insulin receptors and reduced glucose output from the liver.”
Dr. Chhabra said understanding how defective growth hormone receptors prevented diabetes at the cellular and tissue level could enable researchers to develop treatments for the general population.
“Both growth hormone receptors and STAT5 could become targets for new treatments,” he said.
The study was a collaboration between UQ, the University of Melbourne and Boston University and is published in The FASEB Journal.
Wilson disease (copper storage disease) is a rare genetic disorder in which one or more genetic mutations disrupt copper metabolism in the liver. At some point, the liver becomes incapable of eliminating copper with bile, and copper accumulates in the liver, eyes and central nervous system. This results in serious liver damage and neurological problems inter alia. MedUni Vienna researchers led by hepatologist Peter Ferenci have now discovered that a recently described genetic mutation protects against fatty liver – apparently via vitamin A metabolism –and also ensures a better outcome for Wilson disease patients. In future, this finding could prove very useful in the personalised treatment of such patients.
The gene that has been identified is “HSD17B13,” which, according to Ferenci, plays an important role in vitamin A metabolism. Follow-up studies are planned to establish whether Wilson disease patients could benefit from this knowledge and potential treatment through the administration of vitamin A. Overall, this genetic mutation was found in every fourth person (around 26 percent). “We can assume that the HSD17B13 gene plays a critical role in the progression of Wilson disease,” explains Ferenci. “If patients do not have this mutation, their prognosis is poorer. So, in the spirit of precision medicine, we are able to predict much more accurately how the disease will progress.
In a highly regarded study published in Hepatology in 2018, the researchers showed that the protein ATP7B, known as the Wilson disease gene, and of which there are hundreds of mutations, did not provide any definitive information regarding prognosis.
Wilson disease can go undetected for years, and is usually discovered by accident. The age range is huge: The youngest known case in Vienna is a two-year-old child and the oldest patient was 74 years old. Even the symptoms are diverse: The disease can be symptomless for a long time or manifest in the form of severe liver damage, Kayser-Fleischer rings in the eyes (corneal changes) and neurological problems including movement disorders such as twitching or tremor in the limbs or even slurred speech and difficulty in swallowing. “In addition to that, there are often psychiatric disorders such as compulsive behaviours through to psychosis,” adds Ferenci.
Is your face long? Wide? Big nose? Small ears? High forehead?
It’s our faces that characterise how the world sees us, and how we recognise our close friends and family. If you’re lucky enough to be born with a highly symmetrical or a very unique face, perhaps you might have a career as a model or actor.
But how do our faces come about – and what happens when things go awry? We need to look way back to the early stages of life to find out.
From a fertilised cell
Like humans, most creatures throughout the animal kingdom have an instantly recognisable face. Such distinctive features as the trunk of an elephant, the long jaws and abundant sharp teeth of a crocodile, varied shapes and sizes of bird beaks and the unique bill of the platypus are all distinct and recognisable.
Our faces arise during the earliest stages of life. And quite incredibly, the processes that give rise to all these distinctive faces – animal and human – are exceptionally well conserved (that is, haven’t changed much over the course of evolutionary history). Amongst humans and other creatures with backbones (together known as vertebrates), the genes and biological processes that make a face are really very similar.
All animals and humans start out as a fertilised cell. Through thousands of cell divisions, the tissues that will eventually make up the skull, jaws, skin, nerve cells, muscles and blood vessels form and come together to create our face. These are the craniofacial tissues.
The face is among the earliest recognisable features that form in an embryo, with the future eye, nose, ear and tissues that will eventually form the upper and lower jaws all established by about 7-8 weeks in human gestation.
Fusion of two sides
By the sixth week of human development, the major fusion processes of the face have taken place – the two sides of the developing nose will join, both to each other and to the tissue that will become the upper lip. This first fusion (the formation of the “primary palate”) establishes the correct anatomy of the face, and serves as a structural guide for the next major fusion event – that of the secondary, or hard palate.
The hard palate originates as two separate “shelves”, one from the left side of the embryo and one from the right. These shelves elevate and grow together to form one continuous structure, ultimately separating the cavities of the nose and sinuses from that of the mouth. (You can feel this hard palate with your tongue – it’s the roof of your mouth.)
Once these fusion processes are complete (by about week 9 of gestation, still well inside the first trimester), the cells of the face still continue to dynamically move, reshape, and take on functional roles. This includes forming the structural framework of the bones, the delivery of oxygen and nutrients by the blood vessels, and controlling eye and jaw movements by the facial muscles.
The formation of the face – tissues that comprise the future nose and upper lip (red), the sides of the nose (blue) and the upper and lower jaws (green) arise by the 4th week of development (A) and have migrated and fused to form a distinctive ‘face’ by the 8th week of development (D). Credit: New insights into craniofacial morphogenesis, CC BY
Sometimes things go astray
Of course, given the incredible complexity and synchronicity required for all these cells and tissues to end up in the correct space, it is perhaps very surprising that things do not go wrong in craniofacial development more often than they do.
Problems can occur with any cell types that make up the skull, face, blood vessels, muscles, jaws and teeth.
But one of the most common craniofacial defects are palatal clefts, where the hard palate does not fuse correctly, leaving children (roughly 1 in 700 worldwide) with a large gap between their nasal passages and mouth.
Although relatively easily corrected by trained reconstructive surgeons in first-world health care systems, significant ongoing healthcare is still essential.
Services such as speech pathology and psychological counselling are often required. The children also may need medical attention to improve hearing, as problems with middle ear bones often come with other craniofacial defects.
Later surgeries to correct muscular defects do not come cheaply – assuming of course that such surgical and allied health is available to the individual in the first place. This is frequently not the case outside the first world.
Understanding why problems occur
To reduce both the severity and incidence of craniofacial defects, researchers use animal model systems – particularly mouse, chicken, frog and zebrafish embryos – to try and uncover the reasons why these defects occur.
Of all craniofacial defects, 25% are attributed (at least partially) to environmental factors such as smoking, heavy alcohol or drug use, toxic metals and maternal infection (such as salmonella or rubella) during pregnancy.
About 75% of all craniofacial defects are linked to genetic factors. As most of the genes that control craniofacial development in animals also do so in humans, using these animal models helps us better understand human palate development and how specific genes are involved.
Eventually this work may lead to new prevention and treatment strategies, for example supplementing the mother’s diet with beneficial nutrients and vitamins.
An example of such an intervention is the B-vitamin folate, used to reduce neural tube defects such as spina bifida. Mandatory folic acid fortification of food in the USA in 1999-2000 resulted in a 25-30% reduction in severe neural tube defects, clearly an exceptional outcome for newborns and their families.
Through greater understanding of the genetic processes that drive facial growth, further beneficial factors will be identified that can be safely given to pregnant mothers, and give a far better start to life to children that may otherwise be born with a craniofacial disorder.
It is not true that patients treated with deep brain stimulation (DBS) of the subthalamic nucleus make always more impulsive decisions than others, with major effects on their health and safety. This is what emerges from a study conducted by SISSA in association with the hospitals of Trieste and Udine, Italy. Credit: rawpixel on Unsplash
Promises of food, sums of money or entertaining pastimes: it does not matter what the temptation is, a new study shows that patients suffering from Parkinson’s disease who are treated with Deep Brain Stimulation of the subthalamic nucleus are not more impulsive than others when making decisions about a stimulus that they find particularly appealing. “Deep Brain Stimulation” (DBS) is an effective surgical technique widely used to treat symptoms of Parkinson’s disease. However, the same technique can expose patients to changes in behaviour and in decision-making processes, for example towards food. This alteration could make them adopt risk behaviours. And yet, a study, conducted by a team led by Marilena Aiello and Raffaella Rumiati, Director of Laboratorio Neuroscienze e Società of SISSA, in association with the “Ospedali Riuniti” of Trieste and the “Azienda Ospedaliera Universitaria” Santa Maria della Misericordia of Udine and published on Journal of Neurology, has found that these alterations do not seem to affect all forms of decision. To establish this, the scientists devised and conducted an experiment, which placed the patients in front of a crucial choice: have a small prize immediately or a bigger one, later. The results that emerged from the research add an important element to understanding the disease and the benefits and problems of the DBS technique, opening up interesting clinical and research prospects.
Three groups, three rewards, no difference
“Psychiatric problems such as obsessions or compulsive behaviours, like the tendency to assume unjustified risks in play, to be unable to resist the temptation of food and greater impulsivity, are sometimes observed in patients with Parkinson’s disease treated with DBS, a technique which involves implanting electrodes into the subthalamic nucleus of the brain. It is a consolidated treatment that allows the patients who are treated to reduce the doses of drugs they take, but this can have undesirable side-effects on the cognitive and emotional sphere and on behaviour” explains the scientist Marinella Aiello. To study decisional impulsivity in these patients, which could be what lies behind their risk choices, the research group used what is technically called “delay discounting”: “We put three groups of people—the first composed of Parkinson’s sufferers with DBS, one with Parkinson’s sufferers without DBS, a third composed of healthy people—in front of a choice” explain the scientists. “In a computer exercise they could decide whether to have a small reward immediately, in the form of particularly appealing food, money or facilitations for activities they consider pleasurable. Or the same reward, but in larger quantities later. In these tasks, the choice usually depends on the time that passes between one option and the other: if it is very short, delayed gratification is chosen and vice versa. The principle behind this experiment is the following: the more the impulsive trait is present, the more the first choice will always be preferred over the second. We measured their performance in this task”. No difference emerged between the three groups: “Our study confirms that patients with DBS are no more impulsive in this kind of situation and they do not try to find gratifications more hastily than the others. Moreover, for the first time, we have demonstrated that this does not even depend on the type of reward offered to them”.
The results on patients with eating disorders and weight increase
There is more: “It has been shown that injuries to or stimulations of the subthalamic nucleus increase the motivation to gratify oneself with food. And yet, in our study, impulsive decision making has remained unchanged, even in the people who, after the surgery, had gained weight or had eating problems compared with those who had none of these undesirable effects. And this is very interesting scientifically speaking”. Instead, explains Aiello, “an increase in impulsivity is observed in patients with fewer years from DBS surgery, with higher doses of levodopa—substance used to treat the symptoms of Parkinson’s disease—with higher memory performance. By revealing interesting relationships between the therapeutic treatments and specific behaviours of the patients, our results contribute to shedding light on the clinical results of such an important treatment like DBS for Parkinson’s disease”.
