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Listen now: Taking on the great UTI challenge— The Femtech World Podcast

The Femtech World Podcast is back and this month we’re talking UTIs with Giovanna Forte, CEO of Forte Medical, who explains how a lack of standard protocol for urine screening is leaving women at increased risk of anti-microbial resistance.
Urinary tract infections (UTIs) disproportionately affect women, and vast gaps exist in terms of common protocols, diagnosis and treatments. Femtech World editor Sarah Sinclair talks to Giovanna Forte, CEO of Forte Medical, about pioneering a way beyond this global challenge and unlocking the full potential of urine screening.
UTIs are one of the leading causes of life-threatening E. coli bloodstream infections in England, with 20% of blood infections leading to sepsis are a result of untreated UTI. We discuss the link between UTIs and antimicrobial resistance and how women may be disproportionately placed at risk. NHS England says UTIs are a major contributor to the burden of antibiotic resistant infections. Despite how common they are, there’s actually no standard protocol for urine collection when it comes to testing for UTI. As a result around 30% of urine samples are unreliable, with 73% of patients presenting with UTI being treated for a non-existent infection.
Giovanna Forte is CEO of Forte Medical, a company co-founded with her brother, Dr Vincent Forte, a retired GP, forensic physician and medical author. He has developed a device which aims to tackle this issue. While he continued as a full-time GP, Giovanna led seven years of R&D on the prototype Peezy Midstream.
For sixteen years prior to Forte Medical she ran her own highly successful communications agency and now enjoys regular invitations to speak at Imperial College, Imperial Business School, various industry events and within secondary schools hoping to inspire the next generation of entrepreneurs.
We hope you enjoy the episode!
Find out more about the Forte Medical and the Peezy Midstream here
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Common cancer marker may play active role in preventing the disease, study finds

Ki-67, a protein used to measure tumour growth, may also help prevent chromosome errors that drive cancer, a study suggests.
The findings could change how scientists view Ki-67, a marker commonly used in breast cancer and other tumours to assess how quickly cancer cells are growing.
Researchers found the protein may help preserve genome stability by maintaining the structural integrity of centromeres, key parts of chromosomes that help ensure DNA is shared correctly during cell division.
The research was led by professor Paola Vagnarelli at Brunel University of London in collaboration with scientists at the University of Edinburgh and the Technical University of Berlin.
Professor Vagnarelli said: “Doctors already measure Ki-67 to see how aggressive a cancer might be. But our results suggest it is actually helping maintain genome stability.
“That means it may be more than a marker. It could potentially also be a therapeutic target.”
The study examined three proteins that attach to chromosomes during cell division and help rebuild the molecular system that tells each new cell what kind of cell it is.
Every human cell carries identical DNA. What makes a liver cell different from a brain cell is which genes are switched on and which are kept inactive.
When a cell divides, that entire system of switches must be rebuilt. The three proteins involved in this process were Ki-67, Repo-Man and PNUTS.
Vagnarelli’s team developed a method that individually removes each protein from a living cell at the precise point of division. Older techniques could not isolate that moment cleanly.
They found that cells rely on all three proteins to reset themselves after division, but each failed in a different way when removed.
Without PNUTS, gene activity spiralled out of control and thousands of genes switched on at once.
Without Repo-Man, cells escaped safety checkpoints that usually stop damaged or abnormal cells from continuing to divide.
“What we didn’t expect was how clean the separation was,” said Vagnarelli.
Each protein fails in its own specific way. There is no redundancy, no safety net. Which means there are three separate points at which this process can go wrong.
“When the system breaks down, cells can emerge with the wrong number of chromosomes. That condition, called aneuploidy, is seen in disorders such as Down syndrome and in many cancers.
“We also found that these chromosome errors can trigger inflammatory signals inside the cell.”
Aneuploidy means a cell has too many or too few chromosomes, which can disrupt normal growth and function.
Inflammatory signals are chemical messages that can make a cell behave as if it is responding to injury or infection.
“These cells behave almost as if they are under attack,” said Vagnarelli.
“The immune response switches on because the genome is unstable.
“That link between chromosome imbalance and inflammation could help explain patterns we see in several diseases.”
The researchers said the findings may help cancer scientists better understand how chromosome instability, loss of gene regulation and cells dividing before they are ready contribute to tumour growth.
They said understanding the normal machinery that prevents these errors may help researchers find ways to push cancer cells into making mistakes they cannot survive.
“We now have a clearer map of the machinery that resets the cell after division,” said Vagnarelli.
“That knowledge gives us a starting point for thinking about new therapeutic approaches.”
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