Rice on the boil in southern NSW
September 13, 2021
With the rice season set for a superlative start following impressive rains, researchers predict growers will, for the first time this season, sow large areas to the new rice variety, V071.
Bred by the Australian Rice Partnership, a NSW Department of Primary Industries (DPI), SunRice and AgriFutures Australia joint venture, V071 is a semi-dwarf, bold medium-grain rice variety with high yield potential.
DPI research agronomist, Brian Dunn, said V071 offers superior grain yield and cold tolerance compared with Reiziq, a popular semi-dwarf medium grain variety that has elongated grain length.
“Our research shows V071 has strong emergence and establishment vigour with reduced shattering, which will be of interest to growers,” Mr Dunn said.
“Another feature of V071 is that its development continues and does not slow during periods of low temperatures like Reiziq, which is beneficial in cool seasons.”
The DPI rice research team compiled data from several years of agronomy and phenology research experiments to deliver new information on critical sowing times for current varieties, including V071.
Mr Dunn said each field and growing situation has specific characteristics, making some varieties more suitable to their requirements than others.
“It is important to consider all the agronomic characteristics of each variety when selecting those best suited to your field and situation,” he said.
“To minimise the risk of cold conditions reducing grain yield across all crops, we advise growers to grow a mix of varieties, over a range of sowing dates, using a variety of sowing methods.”
DPI, SunRice and Rice Extension continue to work with rice growers and advisers to deliver up-to-date advice.
DPI growing guides for all current NSW rice varieties and supporting rice production Primefacts are available from DPI, Rice Extension and SunRice grower services offices and on the DPI website, https://www.dpi.nsw.gov.au/agriculture/broadacre-crops/summer-crops.
Historic Blue Mountains tunnel a step closer
September 13, 2021
Plans to build Australia’s longest road tunnel between Blackheath and Little Hartley are powering ahead, with a major contract awarded for the environmental assessment.
Deputy Premier and Minister for Regional NSW John Barilaro said AECOM Australia had been selected in a competitive tender process to work on the proposed 11-kilometre tunnel, a central component of the Great Western Highway upgrade between Katoomba and Lithgow.
“This project will transform journeys between the Central West and the East Coast, delivering a safe and more efficient journey for locals, truckies and tourists,” Mr Barilaro said.
“AECOM Australia are industry leaders in their field and bring extensive, demonstrated experience in the environmental assessment of roads and tunnels, having worked on major infrastructure projects, including NorthConnex and the M6 Stage 1.
“They have also demonstrated a comprehensive understanding of the unique and sensitive Blue Mountains environment and will be working to develop rigorous measures to avoid and mitigate impacts from the tunnel work.”
Minister for Regional Transport and Roads Paul Toole said the tunnel would be a game-changer for all motorists driving between Western NSW and Sydney.
“AECOM Australia will now need to ensure that the project includes appropriate measures to protect the Blue Mountains’ natural heritage,” Mr Toole said.
“This critical work will focus on continuing the detailed environmental investigations to confirm the feasibility of a tunnel in this location, and will provide the basis for the Environmental Impact Statement, due for extensive community consultation next year.
“Similar contracts have already been awarded for the east and west sections of the upgrade, so it’s great to see the central section reach that stage too.”
“We’re confident that the assessment will show the feasibility of this ambitious project and that we can build an Australian first right here in the Blue Mountains.”
While designs for Australia’s longest tunnel continue, construction on the east and west sections is set to commence in late 2022.
The $4.5 billion duplication of the Great Western Highway between Katoomba and Lithgow is jointly funded by the Australian and NSW Governments. Construction work is scheduled to start in late 2022, with the tunnel slated to begin construction in 2024.
Scientists claim that overeating is not the primary cause of obesity
September 13, 2021
Statistics from the Centers for Disease Control and Prevention (CDC) show that obesity affects more than 40% of American adults, placing them at higher risk for heart disease, stroke, type 2 diabetes, and certain types of cancer. The USDA's Dietary Guidelines for Americans 2020 -- 2025 further tells us that losing weight "requires adults to reduce the number of calories they get from foods and beverages and increase the amount expended through physical activity."
This approach to weight management is based on the century-old energy balance model which states that weight gain is caused by consuming more energy than we expend. In today's world, surrounded by highly palatable, heavily marketed, cheap processed foods, it's easy for people to eat more calories than they need, an imbalance that is further exacerbated by today's sedentary lifestyles. By this thinking, overeating, coupled with insufficient physical activity, is driving the obesity epidemic. On the other hand, despite decades of public health messaging exhorting people to eat less and exercise more, rates of obesity and obesity-related diseases have steadily risen.
The authors of "The Carbohydrate-Insulin Model: A Physiological Perspective on the Obesity Pandemic," a perspective published in The American Journal of Clinical Nutrition, point to fundamental flaws in the energy balance model, arguing that an alternate model, the carbohydrate-insulin model, better explains obesity and weight gain. Moreover, the carbohydrate-insulin model points the way to more effective, long-lasting weight management strategies.
According to lead author Dr. David Ludwig, Endocrinologist at Boston Children's Hospital and Professor at Harvard Medical School, the energy balance model doesn't help us understand the biological causes of weight gain: "During a growth spurt, for instance, adolescents may increase food intake by 1,000 calories a day. But does their overeating cause the growth spurt or does the growth spurt cause the adolescent to get hungry and overeat?"
In contrast to the energy balance model, the carbohydrate-insulin model makes a bold claim: overeating isn't the main cause of obesity. Instead, the carbohydrate-insulin model lays much of the blame for the current obesity epidemic on modern dietary patterns characterized by excessive consumption of foods with a high glycemic load: in particular, processed, rapidly digestible carbohydrates. These foods cause hormonal responses that fundamentally change our metabolism, driving fat storage, weight gain, and obesity.
When we eat highly processed carbohydrates, the body increases insulin secretion and suppresses glucagon secretion. This, in turn, signals fat cells to store more calories, leaving fewer calories available to fuel muscles and other metabolically active tissues. The brain perceives that the body isn't getting enough energy, which, in turn, leads to feelings of hunger. In addition, metabolism may slow down in the body's attempt to conserve fuel. Thus, we tend to remain hungry, even as we continue to gain excess fat.
To understand the obesity epidemic, we need to consider not only how much we're eating, but also how the foods we eat affect our hormones and metabolism. With its assertion that all calories are alike to the body, the energy balance model misses this critical piece of the puzzle.
While the carbohydrate-insulin model is not new -- its origins date to the early 1900s -- The American Journal of Clinical Nutrition perspective is the most comprehensive formulation of this model to date, authored by a team of 17 internationally recognized scientists, clinical researchers, and public health experts. Collectively, they have summarized the growing body of evidence in support of the carbohydrate-insulin model. Moreover, the authors have identified a series of testable hypotheses that distinguish the two models to guide future research.
Adoption of the carbohydrate-insulin model over the energy-balance model has radical implications for weight management and obesity treatment. Rather than urge people to eat less, a strategy which usually doesn't work in the long run, the carbohydrate-insulin model suggests another path that focuses more on what we eat. According to Dr. Ludwig, "reducing consumption of the rapidly digestible carbohydrates that flooded the food supply during the low-fat diet era lessens the underlying drive to store body fat. As a result, people may lose weight with less hunger and struggle."
The authors acknowledge that further research is needed to conclusively test both models and, perhaps, to generate new models that better fit the evidence. Toward this end, they call for constructive discourse and "collaborations among scientists with diverse viewpoints to test predictions in rigorous and unbiased research."
David S Ludwig, Louis J Aronne, Arne Astrup, Rafael de Cabo, Lewis C Cantley, Mark I Friedman, Steven B Heymsfield, James D Johnson, Janet C King, Ronald M Krauss, Daniel E Lieberman, Gary Taubes, Jeff S Volek, Eric C Westman, Walter C Willett, William S Yancy, Cara B Ebbeling. The carbohydrate-insulin model: a physiological perspective on the obesity pandemic. The American Journal of Clinical Nutrition, 2021; DOI: 10.1093/ajcn/nqab270
Thousands of tiny anchors keep our cells in place (and now we know how)
September 14, 2021: UNSW
This is the first time scientists have been able to see in detail what the anchor’s chain looks like. Photo: Marco Heydecker.
Most of the cells in our bodies – be they bone, muscle or pancreas cells – are locked into the right place with the help of tiny anchors (called ‘focal adhesions’). These strong anchors use protein chains to link the cell to collagen, the protein that gives structure to our body.
The anchors help the cells stay put and, for the most part, resist disruptions to their environment – but if a cell morphs into a cancer cell, the chain can break, letting the cancer spread to other parts of the body.
Now, for the first time, a team of UNSW Sydney scientists have found the specific protein (or link) in the chain responsible for upholding the connection.
The findings, published today in Nature Materials, build on our understanding of cell mechanics – and could help give new directions for cancer research.
“We’ve identified the protein that’s essential for these attachments to function,” says Ms Maria Lastra Cagigas, lead author of the study and Scientia PhD candidate at UNSW Medicine.
“If these attachments fail, the cell could be more prone to moving and invading tissues, like cancer.”
Scientists already knew that cancer weakens cells’ anchors in some way, but they didn’t know exactly how this happens.
One of the reasons it’s been so hard to study this is the miniscule size of the anchor’s chain: it’s only a few nanometres thick – about 1/10,000th the size of a human hair.
The team used specialised 3D cryo-electron microscopy – a powerful imaging technique that uses an electron microscope to create high-resolution images of cells – to identify tropomyosin as the key protein in the chain holding the anchor in place. Cryo-electron microscopy is currently the most powerful technique to look at proteins inside cells, and its development won the Nobel Prize in Chemistry in 2017.
“This is the first time we can actually see in detail what the anchor’s chain looks like,” says Professor Peter Gunning, co-senior author of the study. The team made the findings at UNSW’s Mark Wainwright Electron Microscope Unit, and are the first in the world to use this technique to look at these tropomyosin chains.
“It’s completely new technology.”
The researchers identified tropomyosin’s role in the anchor’s chain by comparing normal cells with cells from bone cancer patients, along with cancer cells created in the laboratory.
They then tried putting the tropomyosin back into the cancer cells – surprisingly, the anchors managed to attach again.
“Looking into the future, we want to learn if we can leverage this knowledge to reduce the invasion of cancer cells,” says Ms Lastra Cagigas.
“In the short term, we could use this information to find out if a cancer has a predisposition to metastasize, which means to move throughout the body.
“In the long term, we could look into it as a potential target in cancer treatment.”
Prof. Gunning and co-senior author Professor Edna Hardeman, who have been researching this field of science for 40 years, say it’s a milestone in understanding cell mechanics.
“It's been a real pleasure to watch this work develop,” says Prof. Gunning, who was recently presented with the 2020 President’s Medal from the Australian and New Zealand Society for Cell and Developmental Biology (ANZSCDB) for his contribution to research into cell mechanics.
“It reinforces what has essentially been a lifetime's work for us: understanding the principles of the architecture of cells.”
A potential drug target
Around 30 per cent of the body is made up of collagen, which forms what’s called ‘the matrix’.
“The matrix is like a scaffold present in our bones, ligaments, muscles, and skin. It’s almost everywhere in the body,” says Ms Lastra Cagigas. “Other than the cells that move through our body, like those in blood, the collagen matrix forms the home for most cells – including cancer cells.”
Pancreatic cancer is one of a few cancers that can modify this matrix for its own benefit by creating a ‘barrier’ around the tumour. This barrier works as a defence mechanism, making it harder for cancer treatments like chemotherapy and immunotherapy to kill the cancer cells.
The tumour forces pancreatic cancer-associated fibroblasts (or PCAFs) – cells around the tumour that are anchored by chains – to build this defence barrier. But now that scientists have identified the proteins in the cell’s anchor and chain, they can explore these proteins as future targets for therapies that could loosen that barrier.
“We’ve identified that the type of protein involved in the chain, tropomyosin, is druggable,” says Prof. Hardeman.
“This means it’s possible to develop small molecule inhibitors, or drugs, that can actually attack these proteins.”
Prof. Hardeman says it’s likely that these potential future drugs would be delivered alongside cancer treatments, so the drugs can temporarily destabilise the barrier while the cancer treatments do their work.
A fibroblast cell (shown here in green) in the process of attaching to the collagen matrix (pink). The tropomyosin filaments (blue) are essential to forging – and keeping – this connection. Image: Maria Lastra Cagigas & Michael Carnell / Katharina Gaus Light Microscopy Facility.
While the findings are encouraging, Prof. Gunning says it doesn’t mean suitable drugs will be available for use in the next few years.
“We have an understanding of the biology, but to go from that to treating a patient is difficult to predict,” he says.
“We can see what the path looks like, but we are less sure of the timeline.”
It’s more likely that in the near future – potentially the next two or three years – the protein in the chain, tropomyosin, may help scientists predict which cancers are likely to spread more quickly.
“As we build on the underlying mechanisms of cancer and expand our markers of cancer cell biology, our discovery adds a missing link to the development of a personalised diagnosis for cancer,” says Prof. Gunning.
Disclaimer: Prof. Peter Gunning and Prof. Edna Hardeman have established a company that is developing drugs that target the tropomyosins for a number of health conditions. While drug development was not explored in the research paper, future possibilities of this research, including potential drug developments, are mentioned in this press release.
COVID-19 killing coating a spray away
September 15, 2021
An antiviral surface coating technology sprayed on face masks could provide an extra layer of protection against COVID-19 and the flu.
The coating developed at The University of Queensland has already proven effective in killing the virus that causes COVID-19, and shows promise as a barrier against transmission on surfaces and face masks.
UQ’s Australian Institute for Bioengineering and Nanotechnology researcher Professor Michael Monteiro said the water-based coating deployed worm-like structures that attack the virus.
“When surgical masks were sprayed with these ‘nanoworms’, it resulted in complete inactivation of the Alpha variant of Sars-CoV-2 and influenza A,” Professor Monteiro said.
The coating was developed with Boeing as a joint research project, and was tested at the Peter Doherty Institute for Infection and Immunity at The University of Melbourne.
“These polymer ‘nanoworms’ rupture the membrane of virus droplets transmitted through coughing, sneezing or saliva and damage their RNA,” Professor Monteiro said.
“The chemistry involved is versatile, so the coating can be readily redesigned to target emerging viruses and aid in controlling future pandemics.”
Professor Monteiro said face masks would continue to be an important part of helping prevent or reduce community transmission of COVID-19.
“Antiviral coatings applied on mask surfaces could reduce infection and provide long-lasting control measures to eliminate both surface and aerosolised transmission,” he said.
“We know that COVID-19 remains infectious for many hours or days on some surfaces, and provides a direct route to infection.
“Therefore, there is greater emphasis on eliminating both surface and airborne transmission to complement vaccination of the population to stop the current pandemic.”
The coating is environmentally friendly, water-based and its synthesis aligns with manufacturing techniques used in the paint and coatings industry.
The research, Water-Borne Nanocoating for Rapid Inactivation of SARS-CoV-2 and Other Viruses, is published in ACS Nano (doi.org/10.1021/acsnano.1c05075)
Professor Michael Monteiro
World-first 3D imaging for melanoma detection
September 13, 2021
Queenslanders could have skin cancer diagnosed earlier using world-first 3D scanning technology with the launch of the Australian Cancer Research Foundation Australian Centre of Excellence in Melanoma Imaging and Diagnosis.
University of Queensland Dermatologist Professor H. Peter Soyer said the technology enabled researchers to track moles and skin spots over time using full body mapping, making it a game-changer for melanoma detection.
“This technology is revolutionising early melanoma detection using 3D state-of-the-art body imaging systems that take an image in milliseconds,” Professor Soyer said.
“The telemedicine network allows dermatologists and medical professionals to detect skin cancers remotely, even from the other side of the country.
“For the first time, medical researchers can access a national database of up to 100,000 patient images taken by 3D full body imaging systems located in Queensland, NSW and Victoria, as part of the world’s largest melanoma imaging trial, which aims to develop more efficient and effective screening for the early detection of skin cancer.
“Using algorithms created by artificial intelligence, the 3D imaging systems are able to analyse the images and produce a full body skin spot map, which transforms the way we will monitor patients in the future.”
Australia has the highest rates of melanoma in the world with an average 28,000 Australians diagnosed with the disease every year.
ACRF chief executive officer Kerry Strydom said the Australian Cancer Research Foundation backed the best in research and cutting-edge technology to drive innovation and help create the new Centre.
“Melanoma is a deadly problem that needs disruptive solutions, and ACRF is proud to be to be involved in delivering revolutionary research through this pioneering program,” Mr Strydom said.
The project brings together three leading Australian universities in skin research, UQ, The University of Sydney and Melbourne’s Monash University, to form the interconnected Centre of Excellence in Diagnostic Imaging of Early Melanoma.
Queenslanders can sign up here to be part of the world’s largest melanoma imaging trial using the 3D full body imaging system located at Brisbane’s Princess Alexandra Hospital.
The 3D technology is expected to be rolled out to five other regions across Queensland.
Koala killer being passed to joeys from mum
A deadly koala virus that can cause immune depletion and cancer, known as koala retrovirus, is being transferred to joeys from their mothers, according to University of Queensland scientists.
Associate Professor Keith Chappell, from UQ's School of Chemistry and Molecular Biosciences, said the virus predisposes koala to chlamydia and other disease, and is having a large impact on our wild koala populations across Queensland and New South Wales.
"Koala retrovirus -- also known as KoRV -- and associated diseases are another threat facing koalas, along with climate change and habitat loss.
"The virus causes immune depletion, likely making it much harder for koalas to cope with these other, already-detrimental environmental stressors.
"All northern koalas share a single highly conserved version of KoRV that is integrated into the koala genome, however until now, we weren't certain how other disease-causing variants are spread.
"By sequencing variations of the virus DNA in 109 captive koalas, we finally revealed how the virus spreads -- from mother to joey.
"It seems that transmission between mother and joey likely occurs due to close proximity, via a joey's exposure to a mother's potentially infectious fluids, like their milk.
"Mothers were sharing their virus variants three times more than fathers, suggesting this is the dominant pathway of spread for the virus.
"And, unlike other diseases affecting koalas like chlamydia, there's no evidence of sexual transmission."
The 109 koalas were housed in two sites in south-east Queensland, helping identify a total of 421 unique koala retrovirus sequences.
Collaborator and lead author, PhD candidate Briony Joyce said the research may lead to a re-think in how conservation plans are executed.
"This work will be highly informative for koala conservation, as it suggests that captive breeding programs focused on mothers that have a low amount of retrovirus variants, could result in healthier animals for release," Ms Joyce said.
"Also, we propose that antiretroviral treatment -- if shown to be safe in koala and effective against KoRV -- could be used specifically in mothers during breeding seasons to prevent transmission.
"This work helps pave the way for evidence-based conservation, increasing koala resilience to help them cope with a changing and challenging environment.
"We must do everything we can to ensure the survival of this culturally important species."
Briony A. Joyce, Michaela D. J. Blyton, Stephen D. Johnston, Paul R. Young, and Keith J. Chappell. Koala retrovirus genetic diversity and transmission dynamics within captive koala populations. PNAS, 2021 DOI: 10.1073/pnas.2024021118
Disclaimer: These articles are not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of Pittwater Online News or its staff.