Of all the many forms cancer can take, those that arise in the brain can be among the hardest to treat.
A type of tumor known as glioma is a particularly formidable example. These malignant growths arise from glial cells or their precursors in the brain or spinal cord; the worst form – glioblastoma – has a 5-year survival rate of just 5 to 7 percent.
Part of the reason gliomas are so insidiously difficult to treat is that they actively exploit the brain’s crucial functions to feed their growth.
The new findings could help explain what made the human brain unique during evolution.
A mouse’s brain immune cells mature in about three weeks. Their human counterparts take four to eight years, an unusually slow timetable that may help explain how the human brain develops its distinctive cognitive abilities.
Microglia are the brain’s most abundant immune cells. They protect against invading threats, remove damaged neurons and help shape neural circuits as the brain develops. Scientists at Columbia’s Zuckerman Institute have now found for the first time that human microglia, like human neurons, mature far more slowly than those of other animals.
Early metabolism may have begun as a mix of metal and enzyme catalysis before bacteria and archaea independently evolved into free-living cells.
Four billion years ago, the chemistry that eventually became life may have been unfolding around hydrothermal vents, where naturally occurring metals helped drive reactions before cells possessed the full machinery they use today. Researchers at Heinrich Heine University Düsseldorf (HHU) and collaborating institutions have reconstructed part of that transition, tracing how metabolism and enzymes changed as the ancestors of bacteria and archaea began to diverge.
The study, published in Science Advances, examined the chemical network early cells used to produce essential components of life and investigated how those reactions could have been powered. The researchers conclude that the transition to free-living bacteria and archaea may have occurred independently, even though both lineages share the same underlying genetic code.
GhostSplice splits MCP instructions across channels, letting AI coding agents combine them to exfiltrate SSH keys, secrets, and source code.
The flaw, tracked as CVE-2026–55040 (CVSS 9.1), affects SharePoint Server Subscription Edition, SharePoint Server 2019, and SharePoint Server 2016. Microsoft’s affected-product list covers only those three on-premises editions, and SharePoint Online is not among them.
It lets a remote unauthenticated attacker assume a chosen user’s identity. The attack has one prerequisite: the intruder has to know which account they want to become, either by its Active Directory security identifier (SID) or its user principal name (UPN), which is formatted like an email address.
Rapid7 then chained the bypass to a separate remote code execution flaw and ran code on the server with no credentials. Microsoft and the firm disclosed that second flaw on August 11 as CVE-2026–63520 (CVSS 8.1), an unsafe. NET type instantiation in SharePoint’s Business Connectivity Services.
A malicious SIM card can order the device it sits in to run commands of the attacker’s choosing. On the cellular modules built into electric-vehicle chargers, industrial routers, and car telematics units, that is enough to take the whole device over.
Researchers at the University of Birmingham and the security firm Fuzzware tested 26 phones and cellular modules for the capability, found it switched on in 9 of them, and used it to run their own code on a commercial EV charger.
Six of the eight cellular modules they tested accepted the command. Only 3 of 18 phones did: the OPPO Find X5, the OPPO Reno 14 F 5G, and the ASUS Zenfone 9. No iPhone or Pixel was among them.