SEATTLE – Ten years after "Berlin patient" Timothy Ray Brown, a second patient has achieved long-term undetectable viral load in the absence of antiretroviral treatment (ART) after receiving a bone marrow transplant with hematopoietic stem cells with a nonfunctional version of the CCR5 receptor, a surface molecule on helper T cells that is used as an entry co-receptor by HIV.
Sleep is universal on both the species and the individual level. Though there have been reports of individuals, both in humans and other species, who need almost no sleep, a truly sleepless individual has never been identified.
Preventing off-target effects of CRISPR/Cas9 remains a major obstacle to the genome editing method's clinical application. In fact, even predicting when and where off-target effects will occur presently remains an imprecise undertaking at best. Researchers from Astrazeneca plc and Imperial College London have developed a molecular-precision tool for DNA manipulation that allowed them to demonstrate that CRISPR's off-target effects increased as DNA was physically stretched.
Sleep is universal on both the species and the individual level. Though there have been reports of individuals, both in humans and other species, who need almost no sleep, a truly sleepless individual has never been identified.
Scientists at the Technical University of Munich have demonstrated that sodium chloride increased the responses of T helper 2 (TH2) cells through several different mechanisms.
Blocking the CCR5 receptor on neurons enhanced the recovery from stroke and traumatic brain injury in animal studies, and patients with the delta32 mutation in CCR5, which renders the receptor nonfunctional, showed better recovery after mild to moderate stroke in the TABASCO clinical trial.
In findings that show a way to target tumors with mutations in isocitrate dehydrogenase 1 (IDH1), as well as bring new insights into the complexity of its effects, researchers have discovered that inhibiting cell cycle checkpoints or the DNA damage response could be a treatment option for gliomas with IDH1 mutations.
Researchers at the University of Wisconsin have discovered a link between fragile X syndrome (FXS) and Huntingtin (Htt) protein, better known for its role in Huntington's disease (HD).
