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A 70-year-old man presented to the emergency department with a painful exacerbation of right trigeminal neuralgia, managed for 5 years with carbamazepine. Clinical examination revealed binocular diplopia due to an abduction deficit in the right eye and hypoesthesia in all divisions of the right trigeminal nerve (V1, V2, V3), without clinical signs of right VII or VIII cranial nerve involvement. High-resolution 3D T2-weighted steady-state MRI (Figure) revealed vertebrobasilar dolichoectasia (VD) with deviation of the right fifth cranial nerve root, complete atrophy of the right sixth cranial nerve, and deviation of the right acoustic-facial nerve bundle.

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Although VD mainly causes ischemic stroke or brainstem compression, cranial nerve involvement is rare. Abducens nerve compression is exceptional, with 11 cases reported up to 2020,1 and combined fifth and sixth nerve involvement even rarer (2 cases).2.

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A new USC study suggests that gut imbalances in children with autism may create an imbalance of metabolites in the digestive system—ultimately disrupting neurotransmitter production and influencing behavioral symptoms.

The research, published in Nature Communications, adds to a growing body of science implicating the “gut-brain” axis in . The discovery raises the possibility of new treatment avenues. It’s an example of how research at USC, and other universities, drives innovation and leads to discoveries that improve lives.

“We demonstrated that gut metabolites impact the brain, and the brain, in turn, affects behavior. Essentially, the brain acts as the intermediary between gut health and autism-related behaviors,” said first author Lisa Aziz-Zadeh, a professor at the Brain and Creativity Institute at the USC Dornsife College of Letters, Arts and Sciences.

Despite major therapeutic advances in the treatment of acute lymphoblastic leukemia (ALL), resistances and long-term toxicities still pose significant challenges. Cyclins and their associated cyclin-dependent kinases are one focus of cancer research when looking for targeted therapies. We discovered cyclin C to be a key factor for B-cell ALL (B-ALL) development and maintenance. While cyclin C is not essential for normal hematopoiesis, CcncΔ/Δ BCR::ABL1 + B-ALL cells fail to elicit leukemia in mice. RNA sequencing experiments revealed a p53 pathway deregulation in CcncΔ/Δ BCR::ABL1 + cells resulting in the inability of the leukemic cells to adequately respond to stress. A genome-wide CRISPR/Cas9 loss-of-function screen supplemented with additional knock-outs unveiled a dependency of human B-lymphoid cell lines on CCNC. High cyclin C levels in B-cell precursor (BCP) ALL patients were associated with poor event-free survival and increased risk of early disease recurrence after remission. Our findings highlight cyclin C as a potential therapeutic target for B-ALL, particularly to enhance cancer cell sensitivity to stress and chemotherapy.

The Philadelphia (Ph) chromosome, a product of the reciprocal translocation t(9;22)(q34;q11) between chromosomes 9 and 22, encodes the BCR::ABL1 fusion oncoprotein.1 The constitutively active BCR::ABL1 tyrosine kinase is a hallmark of chronic myeloid leukemia (CML) and drives a subset of acute lymphoblastic leukemia (ALL). The incidence of Ph positive (Ph+) ALL correlates with age, from only 3% in pediatric ALL to around 25% in older adults.2 Direct targeting of the BCR::ABL1 kinase with tyrosine kinase inhibitors (TKI) has been a breakthrough in targeted cancer therapy. Despite efforts to counteract TKI resistance and improve safety profiles, refractory BCR::ABL1+ leukemia, as well as toxicities and long-term side effects of TKI, present particular therapeutic challenges.3–5

The clinical relevance of cyclins and their associated cyclin-dependent kinases (CDK) has been a major focus of research for several years. Cyclin-CDK complexes do not only drive the cell cycle, but are also important players in various other cellular processes including transcriptional and epigenetic regulation, metabolism or stem cell self-renewal.6 In line with their importance in different pathways, cyclin-CDK complex dysregulation is implicated in many different types of cancer.7

A car accident, football game, or even a bad fall can lead to a serious or fatal head injury. Annually, traumatic brain injuries (TBI) cause half a million permanent disabilities and 50,000 deaths. Monitoring pressure inside the skull is key to treating TBI and preventing long-lasting complications.

Most of these monitoring devices are large and invasive, requiring surgical emplacement. But Georgia Tech researchers have recently created a sensor smaller than a dime. The miniature size offers huge benefits.

“Surgery means extensive recovery time and can significantly impact . Our system doesn’t require surgery because we use a conventional stent, the catheter, as a delivery vehicle,” said W. Hong Yeo, the Harris Saunders Jr. Endowed Professor and an associate professor in the George W. Woodruff School of Mechanical Engineering.

Developing humanoid robots, unravelling the complexities of AI, and the mysteries of consciousness.

Welcome to the ⁠⁠⁠North of Patient⁠⁠⁠ podcast — conversations on health[beyond]care — where we paint an inspired landscape of healthcare’s future through dialogues with creative and unconventional thinkers from around the world.

For a summary of the episode, visit the ⁠blog post⁠ on North of Patient:
https://open.substack.com/pub/northofpatient/p/episode-13-dr…Share=true.

This week’s guest is the remarkable Dr. Suzanne Gildert. She’s a physicist, artist, and AI tech executive based in Vancouver on a mission to uncover the mysteries of consciousness and innovate unconscious AI.

In this episode, we dive into the groundbreaking advancements and pressing challenges in quantum computing, examining the transformative potential of these technologies to reshape our world. Beyond the science, we also explore the philosophical dimensions of AI consciousness, questioning whether AI can ever truly replicate human experience and identity.

Learn more about Nirvanic AI:

Scientists from Mass General Brigham and Beth Israel Deaconess Medical Center have developed a novel gene editing tool called STITCHR. Unlike traditional CRISPR, STITCHR inserts entire genes at precise locations, minimizing unintended mutations. This gene editing tool simplifies use and offers potential as a one-time treatment for genetic disorders.

The technology uses retrotransposons, naturally occurring “jumping genes” found in all eukaryotic organisms, which can move and integrate into genomes. Using computational screening, the researchers identified and reprogrammed a specific retrotransposon to work with the nickase enzyme from CRISPR, forming the complete STITCHR system that allows a precise, seamless gene insertion into the genome.

STITCHR offers the potential to replace or supplement entire genes, creating a more universal treatment option for various genetic diseases. The research team is now working to improve its efficiency and move it toward clinical use. Their study, published in Nature, highlights how insights from basic cellular biology can drive innovation in genetic medicine and lead to new therapeutic tools.

While CRISPR-mediated gene editing has led to powerful advances across biology, medicine, and agriculture, challenges persist in optimizing the editing efficiency of enzymes, such as the widely used Cas9 nuclease. This is especially true in therapeutic use cases, where the goal is to attain high rates of editing via a relatively low and transient enzyme dose.

In a new study published in the April 2025 issue of The CRISPR Journal titled, “Hairpin Internal Nuclear Localization Signals in CRISPR-Cas9 Enhance Editing in Primary Human Lymphocytes,” researchers from the Innovative Genomics Institute (IGI) at the University of California (UC), Berkeley, present a strategy to improve editing efficiency in human immune cells for therapeutic applications by leveraging new constructs for nuclear localization signal (NLS) sequences.

“Efficient CRISPR enzyme production is essential for translation. This is one element that allowed the rapid clinical evaluation of Casgevy, the world’s first genome editing drug. Unfortunately, this aspect tends to be overlooked in the basic research performed in academia,” said Ross Wilson, PhD, assistant adjunct professor of molecular and cell biology at UC Berkeley, who led the new study.