Brief description not available

Brief description not available

Brief description not available

Brief description not available

Cortisol is an essential steroid hormone that is involved in numerous physiological processes such as the stress response, regulation of blood pressure, immune modulation, and regulation of the sleep cycle. Cortisol levels can vary based on several factors. Cortisol imbalances can indicate adrenal disorders, such as Cushing’s Syndrome and Addison’s Disease. Cortisol imbalance can also lead to disruption in the sleep cycle, increased stress, and metabolic disorders. Given these facts, accurate and accessible cortisol monitoring is crucial for diagnostics and overall health.Standard methods for monitoring cortisol levels involve enzyme-linked immunosorbent assays or liquid chromatography-tandem mass spectrometry. These methods, while reliable are performed in laboratory settings using expensive equipment and take significant time to produce results. Reliable on-site or at-home detection methods of cor are unavailable, but would be important tools

Professor Linlin Zhao and their team from the University of California, Riverside have developed mTAP, a new chemical probe engineered to selectively bind to abasic sites within mitochondrial DNA without affecting nuclear DNA. Unlike non-specific agents, mTAP is equipped with a mitochondria-targeting group, ensuring its precise localization. This invention is advantageous over current technology because its mechanism of action involves forming a stable chemical bond with damaged DNA sites, thereby protecting mtDNA from enzymatic cleavage and maintaining its replication and transcriptional activities.    Fig 1: The UCR mitochondria-targeting water-soluble probe mTAP exclusively reacts with mitochondrial abasic sites, and retains mitochondrial DNA levels under genotoxic stress which are responsible for certain mitochondrial diseases. 

A standalone, low-cost robotic device that quantitatively assesses and intensively trains thumb proprioception to enhance motor recovery after neurological injury.

Huntingtin disease (HD) is a heritable neurodegenerative disorder affecting up to 1 in 10,000 people, with an average survival duration of 17-20 years post symptom onset. HD patients typically suffer from severe motor/coordination decline and weight loss. There is no cure for HD, and traditional small molecule drugs only address symptom management. Prior approaches to treatment have failed for several reasons. Protein-targeting approaches such as ubiquitin ligase lack specificity, degrading both mutant and wild type huntingtin protein indiscriminately. Other approaches such as antisense oligonucleotides (ASOs) can target mutant RNA but require many doses over the patient’s lifetime. The disorder affects the huntingtin gene (HTT), which is essential in transcription, reactive oxygen species detection, DNA damage repair, and axonal transport. HD is caused by a heterozygous polyglutamine repeat expansion in exon 1 of HTT. Genome editing is an attractive alternative therapy for HD, as it would require a single dose and is permanent. UC Berkeley researchers have developed a system for CRISPR-based genome editing for genetic diseases like HD. Allele specific excision is possible through two different mechanisms: heterozygous SNPs that create/remove a PAM site, and heterozygous SNPs that create a mismatch within the seed region. For patients with these genotypes, the invention allows selective excision of the pathogenic repeats from only that allele. Over 20% of HD patients can be treated with just one of our novel candidate pairs, and about half of all patients could benefit from one of our novel candidate pairs.