The University of the Free State (UFS) and the Free State Department of Health are not just introducing new technology, but embarking on a journey that will revolutionize surgery and patient care in the region. This is the message delivered by MaQueen Letsoha-Mathae, Premier of the Free State, during the official launch of the Versius Surgical Robotic System on 11 March 2025 at the UFS Faculty of Health Sciences. The Free State is now the first region in Southern Africa to implement this technology, having successfully completed nine robotic-assisted surgeries at Universitas Academic Hospital within the last month.

The successful procedures, which took place between 24 February and 6 March, included complex surgeries such as radical prostatectomies and cholecystectomies, demonstrating the Versius system’s potential to improve patient outcomes. Prof Freddie Claassen, Academic Head of the Department of Urology at UFS and Universitas Hospital, was among the first surgeons from the university to be trained on the system and use it in operations.

A Significant Milestone

“This moment marks a significant milestone not only for our beloved Free State, but for the entire health-care landscape in Southern Africa. We are not merely launching a new technology; we are embarking on a journey that will transform the future of surgery and patient care in our province and beyond,” said Letsoha-Mathae.

She emphasized that the introduction of the Versius Surgical Robotic System aligns with the Free State’s vision to become a hub of healthcare innovation and excellence in Southern Africa. “With this groundbreaking system, we are not only enhancing surgical precision, but also significantly improving patient outcomes,” Letsoha-Mathae added.

The Versius Surgical Robotic System is known for its versatility and adaptability, seamlessly integrating into any operating room. It can be used in high-specialty procedures, including thoracic, colorectal, general and upper gastrointestinal, hernia, gynaecology, and urology surgeries.

Prof Hester C. Klopper, Vice-Chancellor and Principal of UFS, reflected on the role of the university in shaping the future of healthcare. “This moment is not just a technological milestone, but a symbol of what we can achieve as an institution when we unite academic excellence, visionary leadership, and a commitment to community impact with partners in the private sector and government,” she said.

She stressed that the launch reaffirms UFS’s ongoing dedication to academic excellence, technological innovation, and societal impact, while addressing some of the most pressing healthcare challenges both regionally and globally. “Versius is an investment in the well-being of our communities and an essential step towards bridging the healthcare gap in our region,” said Prof Klopper.

Enhancing Surgical Precision

Prof Vasu Reddy, Deputy Vice-Chancellor of Research and Internationalisation at UFS, explained the significant benefits of robotic-assisted surgeries. “Robots such as the Versius system are tools that enhance the senses and skills of surgeons during delicate operations. Unlike traditional surgery, which requires large incisions, robotic surgery enables doctors to perform operations with smaller cuts, reduced pain, and less scarring,” he said.

Robotic surgery improves surgical outcomes by allowing for greater precision, accuracy, and reduced chances of complications. “The robots do not tire, they do not lose focus, and they can handle repetitive tasks with ease, making the entire process safer for patients,” Prof Reddy continued. He further highlighted the role of AI and robotics in healthcare, emphasizing that human innovation and machine precision together can elevate the standard of care.

According to Premier Letsoha-Mathae, the Versius Surgical Robotic System represents a significant leap towards enhancing healthcare delivery in Southern Africa. “The benefits of Versius are profound: patients will experience quicker recoveries and an earlier return to work, ultimately leading to a healthier, more productive society,” she said.

The system’s modular and scalable design ensures that it can be integrated into operating rooms with minimal infrastructure changes, making it accessible across both private and state healthcare sectors. This adaptability promises to expand access to robotic-assisted surgery, helping to bridge the gap in healthcare delivery.

Through the collaboration between the Department of Health and UFS, the launch of the Versius Surgical Robotic System is a testament to the shared commitment to addressing regional and global healthcare challenges. It also underscores the importance of continuing innovation and academic excellence in advancing healthcare technology and patient care.

Tuberculosis thrives in the lungs, but when the bacteria causing the disease are expelled into the air, they face a much harsher environment with drastic changes in pH and chemistry. Understanding how these bacteria survive this airborne journey is essential for their persistence, yet little is known about the mechanisms that protect them as they move from one host to another.

Now, MIT researchers and their collaborators have identified a family of genes that are crucial for the bacterium’s survival specifically when exposed to the air, likely offering protection during its transmission.

Previously, many of these genes were thought to be nonessential, as they didn’t appear to affect the bacteria’s role in causing disease when introduced into a host. This new study, however, suggests that these genes are vital for transmission rather than proliferation.

“There is a blind spot in our understanding of airborne transmission, especially regarding how a pathogen survives sudden environmental changes as it circulates in the air,” says Lydia Bourouiba, head of the Fluid Dynamics of Disease Transmission Laboratory, associate professor of civil and environmental engineering, mechanical engineering, and core faculty member at MIT’s Institute for Medical Engineering and Science. “Now, through these genes, we have an insight into the tools tuberculosis uses to protect itself.”

The team’s findings, published this week in Proceedings of the National Academy of Sciences, could lead to new tuberculosis therapies that target both infection and transmission prevention.

“If a drug targeted the products of these genes, it could effectively treat an individual and, even before that person is cured, prevent the infection from spreading,” says Carl Nathan, chair of the Department of Microbiology and Immunology and the R.A. Rees Pritchett Professor of Microbiology at Weill Cornell Medicine.

Nathan and Bourouiba co-senior authored the study, which includes MIT collaborators and Bourouiba’s mentees from the Fluids and Health Network: co-lead author postdoc Xiaoyi Hu, postdoc Eric Shen, and students Robin Jahn and Luc Geurts. The research also involved collaborators from Weill Cornell Medicine, the University of California at San Diego, Rockefeller University, Hackensack Meridian Health, and the University of Washington.

Pathogen’s Perspective

Tuberculosis is a respiratory disease caused by Mycobacterium tuberculosis, a bacterium that predominantly affects the lungs and spreads through droplets released by an infected person, typically when they cough or sneeze. Tuberculosis remains the leading cause of death from infection, except during global viral pandemics.

“In the last century, we’ve seen the 1918 influenza pandemic, the 1981 HIV/AIDS epidemic, and the 2019 SARS-CoV-2 pandemic,” notes Nathan. “Each virus has caused significant loss of life, but after they subsided, we were left with the ‘permanent pandemic’ of tuberculosis.”

Much of the research on tuberculosis focuses on its pathophysiology—how the bacteria infect a host—along with diagnostic and treatment methods. For their new study, Nathan and Bourouiba turned their attention to tuberculosis transmission, specifically exploring how the bacteria defend themselves during airborne transmission.

“This is one of the first efforts to study tuberculosis from an airborne perspective, investigating how the organism survives harsh changes in the environment during transmission,” says Bourouiba.

Critical Defense

At MIT, Bourouiba studies fluid dynamics and how droplet behaviors can spread particles and pathogens. She partnered with Nathan, who investigates tuberculosis and the genes that the bacteria rely on throughout their life cycle.

To explore how tuberculosis survives in the air, the team aimed to replicate the conditions the bacterium encounters during transmission. They first worked to develop a fluid with similar viscosity and droplet sizes to those expelled by a person coughing or sneezing. Bourouiba points out that previous research on tuberculosis relied on liquid solutions that are used to grow the bacteria. However, these liquids differ significantly from the fluids tuberculosis patients expel.

Furthermore, the fluid typically sampled from tuberculosis patients, like sputum for diagnostic tests, is thick and sticky, which makes it inefficient at spreading and forming inhalable droplets. “It’s too gooey to break into inhalable droplets,” Bourouiba explains.

Through her research on fluid and droplet physics, the team determined a more accurate viscosity and droplet size distribution for tuberculosis-laden microdroplets in the air. They also analyzed the composition of droplets by studying infected lung tissue samples. They then created a fluid that mimicked the viscosity, surface tension, and droplet size that would be released into the air when a person exhales.

Next, the team deposited different fluid mixtures onto plates as tiny droplets, measuring how they evaporated and what structures they left behind. They discovered that the new fluid shielded the bacteria at the center of the droplet, unlike traditional fluids where bacteria were more exposed to the air. The realistic fluid also retained more water.

The team then infused the droplets with bacteria carrying genes with various knockdowns to see how the absence of specific genes affected bacterial survival during evaporation.

They evaluated over 4,000 tuberculosis genes and identified a family of genes that became crucial in airborne conditions. Many of these genes are involved in repairing damage to oxidized proteins, such as those exposed to air, while others are responsible for breaking down irreparably damaged proteins.

“What we found is a lengthy list of candidate genes, some more prominently involved than others, that could play a critical role in helping tuberculosis survive during transmission,” Nathan says.

While the experiments cannot fully replicate the bacteria’s biophysical transmission (as droplets fly through the air and evaporate), the team mimicked these conditions by placing plates in a dry chamber to accelerate droplet evaporation, similar to what happens in flight.

Going forward, the researchers are developing platforms to study droplets in flight under various conditions. They plan to further investigate the role of the newly identified genes in more realistic experiments, potentially weakening tuberculosis’s airborne defenses.

“The idea of waiting to diagnose and treat someone with tuberculosis is an inefficient way to stop the pandemic,” Nathan says. “Most individuals who exhale tuberculosis haven’t been diagnosed yet, so we need to interrupt its transmission. Understanding the process is key, and now we have some ideas.”

A new study by researchers at the Rajiv Gandhi Centre for Biotechnology (RGCB), Kerala, India, has revealed a crucial connection between mRNA processing and oxidative stress response, shedding light on a condition that plays a pivotal role in the development of various diseases, including cancer, cardiovascular disorders, neurological diseases, and diabetes, as well as aging. The research emphasizes the critical impact of oxidative stress, particularly in the heart, which contributes to several health conditions such as hypertension, heart failure, hypoxia, ischemia-reperfusion injury, atherosclerosis, and hypertrophy (excessive development of an organ or tissue).

The team of scientists at RGCB, led by Dr. Rakesh S. Laishram (Scientist), Dr. Feba Shaji, and Dr. Jamshaid Ali, discovered that during oxidative stress, when reactive oxidative species exceed the cell’s capacity to neutralize them, the production of antioxidant proteins is boosted. This is achieved by enhancing the fidelity of RNA processing, a mechanism that helps cells combat oxidative stress. The study, published in Redox Biology journal, uncovers this novel pathway in gene expression.

In the gene expression process, DNA is transcribed into RNA, which is then translated into proteins responsible for carrying out various cellular functions. Manipulations in these pathways—whether through DNA, RNA, or proteins—can alter gene expression depending on the cellular state. RNA processing, a key pathway controlling gene expression, involves the cleavage of RNA. Interestingly, this cleavage is not always precise, with multiple potential cleavage sites, a phenomenon known as cleavage heterogeneity.

“Controlling oxidative stress is crucial for maintaining cellular health and preventing human diseases. One key way cells regulate oxidative stress is by controlling gene expression through alterations in DNA, RNA, or proteins,” says Dr. Laishram, highlighting the importance of this research in understanding how cells respond to oxidative stress through imprecisions in RNA processing. “This underscores the therapeutic potential of targeting cleavage precision in RNA to mitigate oxidative stress and its associated pathologies.”

Dr. Chandrabhas Narayana, Director of RGCB, described it a significant contribution to understanding how antioxidants influence the pathogenesis and development of diseases.

While previous research had not fully elucidated the mechanism, regulation, or biological implications of cleavage imprecision, this study challenges the common perception that such imprecision is merely error-prone. Dr. Shaji and her team discovered that cleavage imprecision is tightly regulated, playing a critical role in controlling gene expression in response to oxidative stress. Key oxidative stress response genes, such as NQO1, HMOX1, PRDX1, and CAT, show higher heterogeneity compared to genes involved in non-stress responses. Furthermore, the number of cleavage sites on these RNA molecules is reduced, enabling cells to better respond to oxidative stresses.

The RGCB researchers have now shown that this heterogeneity is driven by a fidelity cleavage complex that cleaves RNA at a primary site during oxidative stress. This study marks the first example of the biological significance of cleavage imprecision, which regulates gene expression in the cellular oxidative stress response. The findings offer a novel mechanism of antioxidant response, distinct from other oxidative stress pathways, with far-reaching implications for understanding the pathogenesis of diseases such as cancer, cardiovascular conditions, inflammation, neurodegeneration, aging, and diabetes.

This breakthrough could pave the way for new therapeutic approaches targeting oxidative stress, offering hope for the treatment of a wide range of diseases where antioxidant responses are vital.