London man in coma after horror Thailand bike crash needs £100k to get home
It's thought that his motorbike was hit head-on by a car, causing a brain hemorrhage. Following emergency brain surgery, Okemena has remained unconscious for nearly a month.
Striving to fund his medical repatriation, the family is gathering donations through GoFundMe. His elder brother, Ibs, 33, expressed the family's desperation: "This is the hardest time of our lives. It's been very stressful. My parents and I flew to Thailand as soon as we heard and have now basically moved here."
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He added: "But trying to find the money for everything is incredibly draining. The hospital bill is already at £70,000 and the cheapest quote we've had for medical repatriation to the UK is a staggering £144,000."
Despite these challenges, they remain committed to exploring every possibility to transfer him back to the UK. There is an uncertainty about whether Okemena had travel insurance, which only adds to the financial and emotional strain on the London-based family.
Ibs said: "We don't know whether or not he had travel insurance and the companies make it too difficult to find out. It's impossible to access the information."
The Sule family have launched a GoFundMe page in an urgent bid to secure £100,000 for medical expenses. Despite collecting £35,745, they find themselves grappling with mounting costs and dwindling time.
Ibs continued: "The support, prayers, and kind messages mean the world to us. But we are still drowning in costs - and time is running out. Any donation, no matter how small, will help keep Okemena alive and ensure he receives the care he urgently needs. If you cannot donate, please share this campaign with your friends and family."
To donate, visit the Sule family's GoFundMe at www.gofundme.com/f/help-save-okemena-urgent-icu-and-brain-surgery-in-thail.
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Yahoo
15 minutes ago
- Yahoo
Why everyone on the internet is suddenly so obsessed with Jet2 Holidays
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Based on facts, either observed and verified firsthand by the reporter, or reported and verified from knowledgeable sources. Newsweek AI is in beta. Translations may contain inaccuracies—please refer to the original content. A promising new drug could help people living with post-traumatic stress disorder (PTSD) finally let go of trauma. This is the discovery of scientists at the Institute of Basic Science (IBS) and Ewha Womans University in South Korea who have identified a new brain mechanism driving the mental health condition—and a drug with the potential to counteract its effects. The team has shown for the first time that "excessive" gamma-aminobutyric acid (GABA)—the brain's primary neurotransmitter—produced by star-shaped support cells in the brain known as "astrocytes" impairs the brain's ability to extinguish fear memories. This inability to forget traumatic memories even after a long period of time is distinct to PTSD and has posed a major hurdle for treatment. 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This astrocyte-derived GABA impaired neural activity, blocking the brain's ability to forget traumatic memories. "This inspired us to investigate astrocytic GABA dysregulation as a potential driver of PTSD pathology, and ultimately, as a novel therapeutic target," said Won. Explaining further how "excessive" GABA in PTSD is produced, he added: "Trauma and stress might increase putrescine metabolism, which raises the levels of MAOB's presubstrate, leading to more GABA production. "At the same time, the enzyme that breaks down GABA, ABAT, is reduced. Together, this combination causes the accumulation of astrocytic GABA and excessive tonic inhibition in key brain regions like the PFC." When the team administered KDS2010, "a highly selective, reversible MAOB inhibitor" developed at IBS, the mice showed normalized brain activity and were able to extinguish fear responses. The promising drug reduced GABA levels, restored blood flow in the mPFC, and re-enabled memory extinction mechanisms. This confirms astrocytic MAOB as a central driver of PTSD symptoms and MAOB inhibition as a viable therapeutic path. The researchers flagged a major challenge of the study was linking clinical findings in humans with cellular mechanisms in the lab. They addressed this by applying a "reverse translational" strategy, beginning with clinical brain scans and moving backward to identify the cellular source of dysfunction. They then confirmed the mechanism and tested drug effects in animal models. This led to a new understanding of how glial cells—non-neuronal cells long thought to be passive—actively shape psychiatric symptoms. Would this type of drug be used alongside other methods like talking therapy for PTSD? "DS2010 alone has a strong potential to restore brain function by normalizing astrocytic GABA and improving fear extinction. However, we think that combining it with psychotherapy, especially exposure-based therapy, could create even greater synergy. By reducing abnormal inhibition in fear extinction circuits, KDS2010 may help the brain become more responsive to therapeutic input," Won explained. How would it be administered? "KDS2010 is an orally available small molecule. In preclinical and early-phase clinical studies, it has been administered once daily in capsule or liquid form. This makes it highly feasible for long-term outpatient use, similar to antidepressants." What about side effects? "In the Phase 1 clinical trial, KDS2010 was found to be well tolerated, with no serious adverse effects reported, even at higher doses. This safety is largely due to its selectivity for MAOB and its reversible mechanism, which avoids the long-term enzyme compensation seen with older MAO inhibitors. Nevertheless, larger trials in PTSD patients will be needed to fully assess tolerability and any rare side effects." Won said the drug is currently undergoing Phase 2 trials for other neurological disorders, which means its safety profile is already being tested extensively in patients. "Because of this, we believe it could reach the public faster than many other new drugs. If future trials for PTSD are successful and regulatory steps proceed smoothly, it could become available within a few years. Importantly, KDS2010 is part of a broader platform that may also be useful for treating other disorders involving astrocytic dysfunction, such as Parkinson's and Alzheimer's disease." Do you have a tip on a health story that Newsweek should be covering? Do you have a question about PTSD? Let us know via health@ Reference Yoon, S., Won, W., Lee, S., Han, K., Ha, E., Lee, J., Hyeon, S. J., Joo, Y., Hong, H., Lee, H., Song, Y., Park, K. D., Huber, B. R., Lee, J., Edden, R. A. E., Suh, M., Ryu, H., Lee, C. J., & Lyoo, I. K. (2025). Astrocytic gamma-aminobutyric acid dysregulation as a therapeutic target for posttraumatic stress disorder. Signal Transduction and Targeted Therapy, 10(1), 240.
Yahoo
42 minutes ago
- Yahoo
Sir Roger Daltrey is afraid he won't make it to the end of The Who tour
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