Lifeboat Foundation

Griffith University researchers have played a key role in using DNA “origami” templates to control the way viruses are assembled.

The global team behind the research, titled “DNA-origami-directed virus capsid polymorphism,” published in Nature Nanotechnology, developed a way to direct the assembly of virus capsids—the protein shell of viruses—at physiological conditions in a precise and programmable manner.

Dr. Frank Sainsbury and Dr. Donna McNeale from the Griffith Institute for Drug Discovery were part of the research team and said forcing viruses to assemble onto DNA folded into different shapes “like origami” was a question that this project answered.

Blood clots can be deadly medical emergencies that can form in different parts of your body. Learn the warning signs that you might have one.

Akash Ingale, was admitted to Fortis Hospital, Vashi, diagnosed with the unusual combination of Myasthenia Gravis and Thymoma. Myasthenia Gravis is a chronic autoimmune neuromuscular disease causing muscle weakness, typically affecting older individuals, making it rare in young patients like Akash. Moreover, the presence of Thymoma in conjunction with Myasthenia Gravis is even rarer, occurring in only 10–12% of cases. For the past eight months, Akash faced significant mobility challenges, severely impacting his quality of life. Managing the conditions required him to be on multiple drug regimens, including steroids and immunosuppressants, further affecting his well-being.

In this video, Dr Prriya Eshpuniyani, Consultant-Thoracic OncoSurgeon Fortis Hospital, Vashi, Navi Mumbai talks about case history, challenges, prognosis.

Painkillers have nasty side effects, such as organ damage or addiction. Researchers have discovered a new drug that may cause none of these.

A common theme among parents and family members caring for a child with the rare Batten disease is “love, hope, cure.” While inspiring levels of love and hope are found among these amazing families, a cure has been more elusive. One reason is rooted in the need for more basic research. Although researchers have identified an altered gene underlying Batten disease, they’ve had difficulty pinpointing where and how the gene’s abnormal protein product malfunctions, especially in cells within the nervous system.

Now, this investment in more basic research has paid off. In a paper just published in the journal Nature Communications, an international research team pinpointed where and how a key cellular process breaks down in the nervous system to cause Batten disease, sometimes referred to as CLN3 disease [1]. While there’s still a long way to go in learning exactly how to overcome the cellular malfunction, the findings mark an important step forward toward developing targeted treatments for Batten disease and progress in the quest for a cure.

The research also offers yet another excellent example of how studying rare diseases helps to advance our fundamental understanding of human biology. It shows that helping those touched by Batten disease can shed a brighter light on basic cellular processes that drive other diseases, rare and common.

Helicobacter pylori (H. pylori) infections are commonly associated with abdominal pain, bloating, and acidity. Clinical evidence suggests that infection with H. pylori cagA⁺ strains dramatically increases the risk of developing gastric cancer.

A specialized protein delivered by H. pylori to the host, oncoprotein “CagA,” has been shown to interact with multiple host proteins and promote gastric carcinogenesis (transformation of normal cells to cancer cells). However, the underlying mechanisms associated with its biochemical activity have not been fully determined yet.

A new study published in Science Signaling on 18 July insights into the additional mechanism of oncogenic CagA action.

Extracellular vesicles in people with nonalcoholic fatty liver disease (NAFLD) encourage colorectal cancers to spread to the liver and prevent immune cells from attacking the metastatic tumors.