Publisher Health

In a breakthrough discovery, published in Nature Communications, scientists from Queen Mary University of London in collaboration with researchers at Newcastle University and The Francis Crick Institute have unraveled the intricate mechanism behind how DnaA, the master initiator of DNA replication in bacteria, specifically opens replication origins, the gateways to DNA duplication. This fundamental understanding sheds light on the crucial process that underpins the growth and reproduction of nearly all bacterial cells.
In this multi-disciplinary work employing single-molecule TIRF microscopy, chemical biology and structural biology, Dr Aravindan Ilangovan, Reader in Structural Biology, and his team at School of Biological and Behavioural Sciences of Queen Mary unveiled the molecular dance of DnaA at the replication origin using cryo-electron microscopy, in detail to near atomic resolution. Their findings reveal a previously unknown dinucleotide binding pocket within the DnaA oligomer, where two bases of a repeating DnaA-trio sequence tightly bind, enabling the capture of a single DNA strand.
“This key single DNA strand capture is the critical step that allows DnaA to pry open the DNA duplex, paving the way for the initiation of DNA replication,” explained Dr Ilangovan. “Our work provides a molecular blueprint for how DnaA orchestrates this crucial step in bacterial replication, a fundamental process that underpins life itself.”
This study’s findings deepen our understanding of DNA replication and hold the potential for therapeutic applications. By targeting the specific interactions between DnaA and the replication origin, researchers could develop novel approaches towards tackling untreatable bacterial infections. Antibiotic resistance is on the rise and there is an ever-increasing need for novel antibiotics to tackle this current crisis.
“This groundbreaking discovery significantly advances our understanding of bacterial replication, a fundamental process crucial for life. The unique mechanism we have unraveled presents a compelling target for developing new antibiotics, potentially leading to novel treatments for multi-antibiotic resistant bacterial infections. We continue to delve deeper into the intricate dance of DNA replication, paving the way for further breakthroughs in understanding bacterial cell biology and combating antibiotic resistance,” concludes Dr Ilangovan.

Losing sleep is actually something to lose sleep about. It doesn’t just make us tired — it can increase anxiety, degrade mood and altogether undermine our emotional functioning, according to a study by University of Houston Professor of Psychology Candice Alfano, who is senior author on the report. The study, published by the American Psychological Association in the journal Psychological Bulletin, synthesized more than 50 years of research on sleep deprivation and mood.
“Emotions govern virtually every aspect of our daily lives, and depriving ourselves of sleep seems to be a sure way to elect a terrible governor. Our findings confirm that even when sleep is only mildly deficient, there are measurable negative changes in how we react to everyday events,” reports Alfano, who is also director of the Sleep and Anxiety Center of Houston. Two of Alfano’s colleagues, Cara Palmer and Joanne Bower, are co-first authors of the report.
“In our largely sleep-deprived society, quantifying the effects of sleep loss on emotion is critical for promoting psychological health,” said Palmer, an assistant professor at Montana State University. “This study represents the most comprehensive synthesis of experimental sleep and emotion research to date, and provides strong evidence that periods of extended wakefulness, shortened sleep duration, and nighttime awakenings adversely influence human emotional functioning.”
The team analyzed data from 154 studies spanning five decades, with 5,715 total participants. In all those studies, researchers disrupted participants’ sleep for one or more nights. In some experiments, participants were kept awake for an extended period. In others, they were allowed a shorter-than-typical amount of sleep, and in others they were periodically awakened throughout the night. Each study also measured at least one emotion-related variable after the sleep manipulation, such as participants’ self-reported mood, their response to emotional stimuli, and measures of depression and anxiety symptoms.
Overall, the researchers found that all three types of sleep loss resulted in fewer positive emotions such as joy, happiness, and contentment among participants, as well as increased anxiety symptoms such as a rapid heart rate and increased worrying.
“This occurred even after short periods of sleep loss, like staying up an hour or two later than usual or after losing just a few hours of sleep,” Palmer said. “We also found that sleep loss increased anxiety symptoms and blunted arousal in response to emotional stimuli.” Findings for symptoms of depression were smaller and less consistent. The findings were also more mixed for negative emotions such as sadness, worry and stress.
Other directions for future research could include examining the effects of multiple nights of sleep loss, looking at individual differences to find out why some people may be more vulnerable than others to the effects of sleep loss, and examining the effects of sleep loss across different cultures, as most of the research in the current study was conducted in the United States and Europe, according to the researchers.
“Research has found that more than 30% of adults and up to 90% of teens don’t get enough sleep,” Palmer said. “The implications of this research for individual and public health are considerable in a largely sleep-deprived society. Industries and sectors prone to sleep loss, such as first responders, pilots, and truck drivers, should develop and adopt policies that prioritize sleep to mitigate against the risks to daytime function and well-being.”

Researchers at the Icahn School of Medicine at Mount Sinai have gained a deeper understanding of the nuanced roles of JAK inhibitors, or modulators, in inflammation across various cell types and tissues. Their findings suggest a more precise approach is required to potentially expand JAK inhibitor use to a wider range of allergy and inflammatory disorders. Details on the findings were published in the December 21, 2023, issue of the journal Cell.
JAK1 is a key protein in the body that supports cell communication and controls the immune system. It is part of a group of proteins that pass signals from a cell’s exterior to its interior. Controlling JAK1 activity is also important in managing conditions such as rheumatoid arthritis and some cancers.
Current JAK inhibitors work well against inflammation in diseases like eczema, but the study suggests a need for a nuanced approach in modulating JAK activity for conditions like asthma. The potential shift toward enhancing, rather than blocking, JAK activity in lung neurons could be a transformative strategy, distinct from traditional JAK inhibitors that mainly target immune cells, say the investigators.
As part of the work, a mouse made with a patient-specific mutation in the gene for JAK1 revealed how this mutant protein causes disease and how it could potentially be harnessed for broader therapeutic use. The study showed that activated JAK1 signaling has tissue-specific effects, including an unexpected immunoregulatory role in lung sensory neurons, where it suppresses lung inflammation.
“This may explain why JAK1-selective inhibitors, while highly successful in atopic dermatitis, have not advanced for asthma treatment and implies that JAK1 signaling has varying or even opposing effects in different cell types and tissues,” says lead study author Brian Kim, MD, MTR, FAAD, the Sol and Clara Kest Professor of Dermatology, Vice Chair for Research, and Director of the Mark Lebwohl Center for Neuroinflammation and Sensation at Icahn Mount Sinai.
The study involved a type of JAK1 gain-of-function (GOF) mutation, first reported by study co-author Stuart Turvey, MBBS, DPHIL, FRCPC in 2017, from patients with an immune dysregulatory and hypereosinophilic syndrome characterized by severe eczema and asthma. A JAK1 GOF mutation is a change in the gene that encodes the JAK1 protein, making it more active than normal. This increased activity can lead to overactive immune responses and may cause health problems like autoimmune diseases or cancer.
“As a pediatrician, I started this work with a commitment to finding a diagnosis and treatment for a family where three members had severe eczema, asthma, and other allergic manifestations. It turned out that they were the first people in the world recognized to have a genetic change causing gain of function of JAK1,” says Dr. Turvey, Professor, Division of Immunology, Department of Pediatrics, Faculty of Medicine, and Canada Research Chair in Pediatric Precision Health, BC Children’s Hospital and The University of British Columbia, Vancouver, Canada. “Today’s publication, led by Dr. Kim and his team at Mount Sinai, is a powerful example of globally collaborative translational research where they started with this single family and have now generated fundamental insights into the interactions between the human immune system and the nervous system. This is precision medicine in practice.”
Previous research by Dr. Kim and his team revealed that JAK1 signaling, typically responsible for regulating immune cells’ inflammatory response, is also present in neurons and controls the sensation of itch. In their new study, Drs. Kim and Turvey created mice with the same genetic mutation as the patients to better understand why JAK1 inhibitors work for some allergy and inflammatory conditions.

In the lung neurons of the mice, the JAK1 mutant protein reduced inflammation caused by exposure to mold by producing substances that suppress inflammation. However, the mice still showed the same skin condition as the original patients, indicating that JAK1 signaling has different effects in different cells and even within the same cell type in different parts of the body.
“Better understanding of JAK signaling in different parts of the body not only helps us discover new things about biology but also gives us a glimpse into how JAK medicines might be used in the evolving landscape of innovative treatments,” says Dr. Kim.
Next, the researchers plan to examine how additional genes along the JAK pathway may also inform tissue-specific patterns of disease. “For example, another protein called STAT6 is further downstream of the JAK1 pathway. Dr. Turvey has found patients with mutations in these genes who also develop similar allergic conditions. However, whether these specific mutations can inform therapeutic strategies for specific diseases remains a very exciting field of inquiry,” says Dr. Kim.

Australian researchers have discovered a new way that epithelial cells, which form layers in organs like the skin and stomach, attach to one another, and how they perceive growth signals at these attachments, helping them form tissues of the right size and shape.
Epithelial cells cover the surfaces of most organs in the body and must adhere to each other to form both a protective and permeable barrier. They are exquisitely designed to both be tightly sealed against pathogens like bacteria, and to also allow the transport of salts, fluids, and nutrients.
Researchers, led by Professor Kieran Harvey and Dr Benjamin Kroeger, at the Monash University Biomedicine Discovery Institute in Melbourne have discovered a new way by which epithelial cells adhere to each other in the vinegar fly, Drosophila. The study is published today in the journal, Developmental Cell.
Previous work from Professor Harvey and others led to the discovery of an important organ growth control pathway, called Hippo. First discovered in Drosophila, the Hippo pathway does effectively the same job in mammals and controls the size of different organs such as the liver and heart. The Hippo pathway is also important for human diseases as it is mutated in multiple epithelial cancers. The new study provides further insights into how Hippo signalling is coordinated in growing tissues.
In the present study, the researchers made the important discovery of a new subcellular adhesion site that helps epithelial cells adhere to one another — termed by the researchers as “basal spot junctions.” They showed that basal spot junctions not only helped cells adhere to one another but were important for regulating Hippo signalling. “Our discovery of basal spot junctions in epithelial tissues has given us new insights into how epithelial cells adhere to each other and how epithelial tissues grow to the right size and shape,” Professor Harvey said.
These latest discoveries of how Hippo signalling operates in growing epithelial tissues are crucially important, according to Professor Harvey, because “when Hippo signalling breaks down, it can cause many types of cancers,” he said.
The first ever Hippo targeted therapies are currently in clinical trials for human cancers and are showing benefit, which “will hopefully lead to better treatments for many types of epithelial cancers like mesothelioma and lung cancer,” Professor Harvey said.

Artery calcification is almost twice as common in night owls compared to early birds, according to a study from the University of Gothenburg, Sweden. Circadian function appears to be particularly important during the early stages of cardiovascular disease.
Atherosclerosis involves fatty deposits accumulating on the inside of the arteries, making it harder for blood to pass through. The disease develops over a very long period of time and is not noticed until it leads to blood clots causing angina, heart attack, or stroke. Previous research has shown that people with late-night habits have an increased risk of cardiovascular disease, but this is the first study to show how circadian rhythms specifically affect calcification of the arteries.
Coronary artery calcification
The study, which has been published in the journal Sleep Medicine, involved 771 men and women aged between 50 and 64, all of whom are part of the larger population study SCAPIS. The degree of artery calcification in the heart’s coronary arteries was examined using computer tomography. Participants themselves indicated their so called chronotype on a five-point scale: extreme morning type, moderate morning type, intermediate type, moderate evening type, or extreme evening type.
Of the 771 participants, 144 identified as extreme morning types, and 128 as extreme evening types. Among the group who were most alert in the morning, 22.2% had pronounced artery calcification — the lowest proportion of all five chronotypes. The extreme evening type group had the highest prevalence of severe coronary artery calcification, at 40.6%.
The first author of the study is Mio Kobayashi Frisk, a doctoral student at Sahlgrenska Academy, University of Gothenburg:
“Our results indicate that extreme evening chronotype may be linked not only to poorer cardiovascular health in general, but also more specifically to calcification in the coronary arteries calcification and atherosclerosis,” Mio Kobayashi Frisk says.

Preventive treatment
The statistical analysis considered a range of other factors that can affect the risk of atherosclerosis, including blood pressure, blood lipids, weight, physical activity, stress level, sleep, and smoking.
The last author of the study is Ding Zou, a researcher at Sahlgrenska Academy, University of Gothenburg:
“As well as the previously known factors, the individual circadian rhythm also appears to be an important risk factor for atherosclerosis. We interpret our results as indicating that circadian rhythms are more significant early in the disease process. It should therefore particularly be considered in the preventive treatment of cardiovascular diseases,” says Ding Zou.
Self-reported chronotype
Those who had experienced a heart attack were excluded from the study, meaning that the study participants were healthier than the general population. Another weakness identified by the researchers is that participants themselves provided their chronotype.
Each chronotype can be said to have an average time when half of the night’s sleep has passed. In a previous study on the same population, though not necessarily the same individuals, this time occurred at 02:55 AM for the extreme morning type group and at 04:25 AM for the extreme evening type group. With the remaining chronotype groups’ mid-sleep times were somewhere in between these extremes.
SCAPIS stands for Swedish CArdioPulmonary bioImage Study. It is a research project within the field of cardiac, vascular, and pulmonary disease. As part of the project, 30,000 randomly selected Swedes aged 50-64 have undergone extensive health examinations: blood sampling, functional tests, and radiological advanced imaging of organs and blood vessels. Six universities and university hospitals are leading and running SCAPIS in close collaboration with the Swedish Heart-Lung Foundation, the study’s main funder.

In Finland, there is a clear increase in the number of sick days taken due to depression, anxiety and sleep disorders in October and November, whereas the number of absences is lower than expected between June and September. In late autumn, the number of sick days taken is almost twice as high as in the summer and about a quarter higher than in early autumn. On the other hand, manic episodes related to bipolar disorder occur more frequently than expected during the spring and summer, when there are more daylight hours, and less frequently than expected during darker times of year.
The results can be found in a study funded by the Research Council of Finland. The study was conducted as a part of the Climate Change and Health research programme. The aim of the study was to investigate the connection between changing light levels and mental health. It is expected that due to climate change, winters in Finland will become darker while summers will become brighter.
During the study, Kela’s sick leave register was used to analyse the seasonal timing of a total of 636,543 sick leaves that were due to mental health reasons over a period of 12 years. The analyses examined whether the expected number of absences was above or below the expected number of sick leaves.
“Previous studies have found that some people experience so-called winter depression (seasonal affective disorder) during the dark season. In addition to the typical symptoms of depression, kaamos depression involves an increased appetite and weight gain along with excess sleepiness, which means sleeping for longer and feeling tired during the day. The symptoms of winter depression can often be alleviated through bright light therapy,” says Timo Partonen, a Research Professor at the Finnish Institute for Health and Welfare.
Seasonal variation can increase workloads in the workplace and in health services particularly in the autumn, when the most common types of sick leaves — absences due to depression, anxiety and sleep disorders — are starting to occur often.
“It’s also worth considering if there are other explanations for the phenomenon apart from a dark season. For example, is there an exceptionally high amount of psychosocial stress in the workplace during autumn, which then leads to an increasing number of sick leaves,” says Professor of Psychology Marianna Virtanen from the University of Eastern Finland.
If climate change causes summers in Finland to become brighter and winters to become darker, the study suggests that depression, anxiety and sleep disorders could increase during the winter because of those changes. However, with the exception of sleep disorders, they could also become less prevalent during the summer. In the case of bipolar disorder, darker winters could alleviate the symptoms of mania, while brighter summers could exacerbate them.

High-frequency terahertz waves have great potential for a number of applications including next-generation medical imaging and communication. Researchers at Linköping University, Sweden, have shown, in a study published in the journal Advanced Science, that the transmission of terahertz light through an aerogel made of cellulose and a conducting polymer can be tuned. This is an important step to unlock more applications for terahertz waves.
The terahertz range covers wavelengths that lie between microwaves and infrared light on the electromagnetic spectrum. It has a very high frequency. Thanks to this, many researchers believe that the terahertz range has great potential for use in space exploration, security technology and communication systems, among other things. In medical imaging, it can also be an interesting substitute for X-ray examinations as the waves can pass through most non-conductive materials without damaging any tissue.
However, there are several technological barriers to overcome before terahertz signals can be widely used. For example, it is difficult to create terahertz radiation in an efficient way and materials that can receive and adjust the transmission of terahertz waves are needed.
Researchers at Linköping University have now developed a material whose absorption of terahertz signals can be turned on and off through a redox reaction. The material is an aerogel, which is one of the world’s lightest solid materials.
“It’s like an adjustable filter for terahertz light. In one state, the electromagnetic signal will not be absorbed and in the other state it can. That property can be useful for long-range signals from space or radar signals,” says Shangzhi Chen, postdoc at the Laboratory of Organic Electronics, LOE, at Linköping University.
The Linköping researchers used a conducting polymer, PEDOT:PSS, and cellulose to create their aerogel. They also designed the aerogel with outdoor applications in mind. It is both water-repellent (hydrophobic) and can be naturally defrosted via heating by sunlight.
Conducting polymers have many advantages over other materials used to create tunable materials. Among other things, they are biocompatible, durable, and have a great ability to be tuned. The tunability comes from the ability to change the charge density in the material. The great advantages of cellulose are the relatively low production cost compared to other similar materials and that it is a renewable material which is key for sustainable applications.
“The transmission of terahertz waves in a broad frequency range could be regulated between around 13 % and 91 %, which is a very large modulation range,” says Chaoyang Kuang, postdoc at LOE.

For decades, it has been known that people with diabetes are at a substantially increased risk of developing severe lung disease if they become infected with viruses such as influenza, as well as with bacteria and fungi. When the COVID-19 pandemic started in early 2020, this mysterious phenomenon gained even more pressing importance: It became clear that people with diabetes were at a significantly higher risk of coming down with severe, even fatal, lung disease after developing a serious form of the virus, but no one understood why. In fact, some 35 percent of people with COVID-19 who died during the pandemic had diabetes.
Now, research conducted at the Weizmann Institute of Science and published in Nature has revealed how, in diabetics, high levels of blood sugar disrupt the function of key cell subsets in the lungs that regulate the immune response. It also identifies a potential strategy for reversing this susceptibility and saving lives.
Prof. Eran Elinav’s team in his lab at Weizmann, headed by Drs. Samuel Nobs, Aleksandra Kolodziejczyk and Suhaib K. Abdeen, subjected multiple mouse models of types 1 and 2 diabetes to a variety of viral lung infections. Just as in diabetic humans, in all these models the diabetic mice developed a severe, fatal lung infection following exposure to lung pathogens such as influenza. The immune reaction, which in nondiabetics eliminates the infection and drives tissue healing, was severely impaired in the diabetic mice, leading to uncontrolled infection, lung damage and eventual death.
Next, to decode the basis of this heightened risk, the team performed an evaluation of gene expression on the level of individual cells, in more than 150,000 single lung cells of infected diabetic and nondiabetic mice. The researchers also performed an extensive array of experiments involving immune and metabolic mechanisms, as well as an in-depth assessment of immune cell gene expression in infected diabetic mice. In the diabetic mice they identified a dysfunction of certain lung dendritic cells, the immune cells that orchestrate a targeted immune response against pathogenic infection. “High blood sugar levels severely disrupt certain subsets of dendritic cells in the lung, preventing these gatekeepers from sending the molecular messages that activate the critically important immune response,” says Nobs, a postdoctoral fellow who was the study’s first author. “As a result, the infection rages on, uncontrolled.”
Importantly, the scientists discovered how high sugar levels in diabetic mice disrupt the normal function of lung dendritic cells during infection. Altered sugar metabolism in these cells led to the accumulation of metabolic byproducts that markedly disrupted the normal regulation of gene expression, leading to aberrant immune protein production. “This could explain why the functioning of these cells is disturbed in diabetes, and why the immune system is unable to generate an effective anti-infection defense,” says Kolodziejczyk, a postdoctoral fellow who co-led the study as a first coauthor.
The scientists next explored ways to prevent the harmful effects of high sugar levels in lung dendritic cells, as a means of lowering the infection’s risk in diabetic animals. Indeed, tight control of blood sugar levels by insulin supplementation prompted the dendritic cells to regain their capacity to generate a protective immune response that could prevent the cascade of events leading to a severe, life-threatening viral lung infection. Alternatively, administration of small molecules reversing the sugar-induced regulatory impairment corrected the dendritic cells’ dysfunction and enabled them to generate a protective immune response despite the presence of high sugar levels.
“Correcting blood sugar levels, or using drugs to reverse the gene regulatory impairment induced by high sugar, enabled our team to get the dendritic cells’ function back to normal,” says Abdeen, a senior intern who co-supervised the study. “This was very exciting because it means that it might be possible to block diabetes-induced susceptibility to viral lung infections and their devastating consequences.”
With over 500 million people around the world affected by diabetes, and with diabetes incidence expected to rise over the next decades, the new research has significant, promising clinical implications.

“Our findings provide, for the first time, an explanation as to why diabetics are more susceptible to respiratory infection,” Elinav says. “Controlling sugar levels may make it possible to reduce this pronounced diabetes-associated risk. In diabetic patients whose sugar levels are not easily normalized, small molecule drugs may correct the gene alterations caused by high sugar levels, potentially alleviating or even preventing severe lung infection. Local administration of such treatments by inhalation may minimize adverse effects while enhancing effectiveness, and merits future human clinical testing.”
Study participants included Dr. Nir Horesh, Dr. Gayatree Mohapatra, Dr. Ryan James Hodgetts, Dr. Igor Spivak, Dr. Leviel Fluhr, Dr. Denise Kviatcovsky, Dr. Mally Dori-Bachash, Dr. Yiming He, Dr. Hagit Shapiro, Christine Botscharnikow, Ella Herzog, Sophia Hejndorf and Sara Ferrini of Weizmann’s Systems Immunology Department; Prof. Ayelet Erez and Lital Adler of Weizmann’s Molecular Cell Biology Department; Prof. Alon Harmelin and Dr. Noa Stettner of Weizmann’s Veterinary Resources Department; Drs. Alexander Brandis and Tevie Mehlman of Weizmann’s Life Sciences Core Facilities Department; Dr. Jens Puschhof and Lena Schorr of the German Cancer Research Center (DKFZ), Heidelberg, Germany; Dr. Arieh Moussaieff and Anish Zacharia of the Hebrew University of Jerusalem; and Prof. Manfred Kopf of the ETH, Zurich, Switzerland.
Prof. Eran Elinav is head of the Belle S. and Irving E. Meller Center for the Biology of Aging. His research is supported by the Swiss Society Institute for Cancer Prevention Research; the Sagol Institute for Longevity Research; the Sagol Weizmann-MIT Bridge Program; the Leona M. and Harry B. Helmsley Charitable Trust; the Mike and Valeria Rosenbloom Foundation; and Miel de Botton.
Prof. Elinav is the incumbent of the Sir Marc and Lady Tania Feldmann Professorial Chair of Immunology. The Vera Rosenberg Schwartz Research Fellow Chair supports a staff scientist in his lab.

Researchers of Karlsruhe Institute of Technology (KIT) and the SMS group have developed a new process to reduce CO2 emission of worldwide steel production by several hundred million tons per year. It is based on modernizing blast furnace technology with moderate investments and has already been demonstrated successfully in a pilot plant. The researchers report in Energy Advances.
About eight percent of worldwide CO2 emissions are produced by steel industry. “This must be changed quickly,” says Professor Olaf Deutschmann from KIT’s Institute for Chemical Technology and Polymer Chemistry (ITCP). He admits that new hydrogen technologies may open up a climate-neutral perspective in the long term. But it will take several years until a sufficient amount of green hydrogen will be available worldwide and new plants will start operation. “We are running out of time in this climate crisis and we have to take countermeasures now.” A new process developed by Deutschmann’s research team in cooperation with the SMS group, Paul Wurth Entwicklungen, and KIT’s startup omegadot has now proved to be effective also in conventional plants. “The potential is very high. We expect that backfitting existing blast furnaces with moderate investments will reduce worldwide direct CO2 emissions by two to four percent,” Deutschmann says.
New Process Reduces Emissions and Saves Energy
The new process departs from iron. This raw material is contained in oxidized form in ores and extracted by means of reduction, i.e. the removal of oxygen, with coke in a blast furnace. Coke does not only produce the energy required for melting, but also serves as a reducing agent in the chemical reaction. “For this special purpose, coke is produced from fossil coal in a highly energy-consuming process,” says Philipp Blanck from ITCP, who cooperated closely with the SMS group at the pilot plant that was part of the steelworks. “In our process, we recycle CO2 from the furnace gas using coke oven gas. This yields a synthesis gas with a large hydrogen fraction that can be used as a coke substitute in the blast furnace.
For backfitting an existing plant, the Cowper heaters must be modified. Then, methane and CO2 from the coke oven gas and CO2 from the blast furnace gas are converted into synthesis gas, a mix of hydrogen and carbon monoxide. This process, so-called dry reforming, requires a high temperature that is mainly taken from the process heat of the blast furnace. The synthesis gas is then blown into the blast furnace to support iron oxide reduction there. “Per ton of steel produced, significant amounts of coke can be saved. Specific CO2 emissions are reduced by up to twelve percent,” Blanck says.
Successful Demonstration in Cooperation with Industry Partners
The process was demonstrated and validated at Dillinger Hüttenwerke, Saarland, in cooperation with omegadot software & consulting GmbH, a startup of KIT. omegadot has developed a software for the precise simulation and visualization of the process and for supporting scale-up to an industrial plant.
The pilot plant in Dillingen is operated by the SMS group together with Dillinger Hüttenwerke and Saarstahl. Operation is aimed at producing steel with reduced CO2 emissions. “Integration of the new process in the steelworks is the first step in the transformation of steel industry,” says Gilles Kass from the Research Section of SMS group, co-author of the publication.

A groundbreaking new technique invented by researchers at the USC Dornsife College of Letters, Arts and Science may revolutionize the field of synthetic biology. Known as CReATiNG (Cloning Reprogramming and Assembling Tiled Natural Genomic DNA), the method offers a simpler and more cost-effective approach to constructing synthetic chromosomes. It could significantly advance genetic engineering and enable a wide range of advances in medicine, biotechnology, biofuel production and even space exploration.
CReATiNG works by cloning and reassembling natural DNA segments from yeast, allowing scientists to create synthetic chromosomes that can replace their native counterparts in cells. The innovative technique enables researchers to combine chromosomes between different yeast strains and species, change chromosome structures, and delete multiple genes simultaneously.
Lead researcher Ian Ehrenreich, professor of biological sciences at USC Dornsife, said the method is a major improvement over current technology. “With CReATiNG, we can genetically reprogram organisms in complex ways previously deemed impossible, even with new tools like CRISPR,” he said. “This opens up a world of possibilities in synthetic biology, enhancing our fundamental understanding of life and paving the way for groundbreaking applications.”
The study was published Dec. 20 in Nature Communications.
CReATiNG makes difficult research easier, cheaper
The field of synthetic biology has emerged as a way for scientists to take control of living cells, such as yeast and bacteria, to better understand how they work and to enable them to produce useful compounds, such as new medicines.
“Over the last decade or so, a new form of synthetic biology has emerged called synthetic genomics, which involves synthesizing whole chromosomes or entire genomes of organisms,” Ehrenreich said. “The thing about most synthetic genomics research is that it involves building chromosomes or genomes from scratch using chemically synthesized DNA pieces. This is a ton of work and extremely expensive.”
However, there have been no alternatives — until now. “CReATiNG offers an opportunity to use natural pieces of DNA as parts to assemble whole chromosomes,” said Agilent postdoctoral fellow Alessandro Coradini, who was study first author.

The method makes advanced genetic research more accessible by significantly lowering costs and technical barriers so scientists can unlock new solutions to some of the most pressing challenges in science and medicine today.
CReATiNG could help medicine, space exploration and more
The findings are particularly significant for their potential applications in biotechnology and medicine. CReATiNG could lead to more efficient production of pharmaceuticals and biofuels, aid in the development of cell therapies for diseases like cancer and pave the way to methods of environmental bioremediation, such as creating bacteria that consume pollutants.
The method might even extend to helping humans live for long periods in space or other harsh environments. Scientists could one day use CReATiNG to develop microorganisms or plants that could thrive in space stations or during long-distance space travel, though the researchers caution that this would require much future research.
One of the most striking aspects of the study, according to the researchers, is how rearranging chromosome segments in yeast can alter their growth rates, with some modifications resulting in up to a 68% faster or slower growth. This discovery highlights the profound impact that genetic structure can have on biological function and opens up new research pathways to further explore these relationships.
About the study
In addition to Ehrenreich and Coradini, authors on the study include Christopher Ne Ville, Zachary Krieger, Joshua Roemer, Cara Hull, Shawn Yang and Daniel Lusk, all of USC Dornsife.
The study was supported by National Science Foundation grant 2124400, National Institutes of Health grant R35GM130381 and an Agilent Postdoctoral Fellowship.