Toggle light / dark theme

Bioengineered neuronal ‘circuit board’ mimics conditions of the human brain

A new bioengineered neuronal circuit board “BioConNet” allows scientists to artificially engineer human brain-like wiring at scale and can be used to engineer any possible circuit. The fully programmable, open-source system allows generation of large-scale circuits, while maintaining the ability to focus on single connections between neurons.

This is a key advance in engineering human-like neural circuits as it allows for a new level of wiring complexity compared to previous systems. BioConNet allows scientists increased control over wiring in the culture compared to existing methods such as organoids and commercially available systems. The research is published in the journal Advanced Healthcare Materials.

“By combining engineering and neurobiology with the most recent stem cell culture techniques, we can now create human-specific, functional, large-scale complex neural circuits in the lab,” said senior author, Dr. Andrea Serio, Reader in Neural Tissue Engineering, Group Leader at the UK Dementia Research Institute (UK DRI) at King’s and Senior Group Leader at the Crick.

Blood test predicts which bladder cancer patients may safely skip surgery

Circulating tumor DNA, or ctDNA, can predict metastatic risk in patients who receive bladder-sparing treatment for muscle-invasive bladder cancer, but it is not a good predictor of local recurrence within the bladder, according to new data presented today by Fox Chase Cancer Center researchers.

The study also showed that the absence of ctDNA predicted favorable outcomes, regardless of whether the patient’s bladder was removed or not. Circulating tumor DNA are tiny fragments of DNA left behind by cancer cells as they die off during treatment.

The study, which reports updated data from the phase 2 RETAIN-2 clinical trial, could be used to help guide treatment decisions for patients with muscle-invasive bladder cancer (MIBC), said first author Pooja Ghatalia, MD, an Associate Professor in the Department of Hematology/Oncology at Fox Chase. She conducted the study with senior author Daniel M. Geynisman, MD, Chief of the Division of Genitourinary Medical Oncology, and a number of other Fox Chase clinicians.

Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy

Among over 7,000 patients with cancer, higher baseline fatigue before systemic therapy was linked to an increased risk of severe, life-threatening, and fatal adverse events.


Question Is baseline patient-reported fatigue associated with subsequent cancer treatment−related adverse events?

Findings In this cohort study and pooled analysis of 7,086 patients from 17 SWOG phase 2 and 3 randomized clinical trials, patients who reported baseline fatigue had a significantly higher risk of severe, life-threatening, and fatal adverse events. In addition, a dose-response pattern was observed, with patients reporting high fatigue vs no fatigue having a nearly 5-fold increased risk of fatal toxic effects.

Meaning Patient fatigue reported before cancer treatment may serve as an early clinical marker of risk for toxic effects and could help guide personalized treatment strategies.

Adherence to Different Dietary Patterns and Subsequent Risk of Total, Ischemic, and Hemorrhagic Stroke

In people with elevated cardiovascular risk at baseline, adherence to the Mediterranean and Mediterranean-DASH Diet Intervention for Neurodegenerative Delay diets was associated with a lower risk of stroke.


BACKGROUND: Adherence to healthy dietary patterns has been related to lower cardiovascular disease risk. However, few studies have examined prospective associations between adherence to different healthy dietary scores and the incidence of stroke and its subtypes. The aim of this study was to prospectively examine the associations between adherence to 4 recognized healthy dietary patterns and the risk of total and ischemic stroke in an existing dietary-based randomized controlled trial. METHODS: This is a secondary observational cohort analysis of 7,447 participants at high cardiovascular disease risk enrolled in the PREDIMED trial (Prevención Con Dieta Mediterranea).

What Can 50-Year-Old Chatbots Teach Us About Clinical Applications of AI?

Can a large language model (LLM) provide insights on the history of chatbots and their clinical applications? 🤖

In this episode of JAMA+ AI Conversations, JAMA+ AI Editor in Chief Roy Perlis, MD, MSc, interviews OpenAI’s ChatGPT (GPT-4o, voice mode) about the development and legacy of the first clinical chatbots, ELIZA and PARRY.

The discussion explores differing perspectives of their creators, as well as how foundational debates about technology and ethics continue to inform the present landscape of AI in mental health care.

🎧 Listen now.


JAMA+ AI Editor in Chief Roy Perlis, MD, MSc, conducted an interview with ChatGPT about the history of chatbots and their clinical applications, for JAMA+ AI Conversations.

Living ‘Mini Brains’ Meet Next-Generation Bioelectronics

A team led by Northwestern University and Shirley Ryan AbilityLab scientists have developed a new technology that can eavesdrop on the hidden electrical dialogues unfolding inside miniature, lab-grown human brain-like tissues, according to a study published the journal Nature Biomedical Engineering.

Known as human neural organoids — and sometimes called “mini brains” — these millimeter-sized structures are powerful models of brain development and disease. But until now, scientists could only record and stimulate activity from a small fraction of their neurons — missing network-wide dynamics that give rise to coordinated rhythms, information processing and the complex patterns of activity that define brain function.

For the first time, the new technology overcomes that stubborn limitation. The soft, three-dimensional (3D) electronic framework wraps around an organoid like a breathable, high-tech mesh. Rather than sampling select regions, it delivers near-complete, shape-conforming coverage with hundreds of miniaturized electrodes. That dense, three-dimensional interfacing enables scientists to map and manipulate neural activity across almost the entire organoid.

Testosterone therapy is associated with reduced risk of acute kidney injury, kidney failure with renal replacement therapy, and cardiovascular events in men with diabetes and hypogonadism

Testosterone deficiency is common in men with diabetes. Effects of testosterone therapy on kidney failure and cardiovascular outcomes in diabetic men remain poorly understood. Our aim was to assess whether testosterone therapy is associated with reduced risk of acute kidney injury and kidney failure requiring replacement therapy in men with diabetes and hypogonadism compared to matched untreated men with diabetes.

Participants were recruited from the TriNetX Research Collaborative network. We identified 26,027 diabetic men with hypogonadism treated with testosterone and matched them 1:1 using propensity score matching to 26,027 untreated diabetic men with hypogonadism. Primary outcomes were acute kidney injury and kidney failure requiring replacement therapy (dialysis or transplantation). Secondary outcomes included myocardial infarction, ischemic stroke, atrial fibrillation, and all-cause mortality. Cox proportional hazard models were used over a mean follow-up of 3.3 years.

Men had a mean age of 58 years (SD 12), with 71% being non-Hispanic White. Testosterone-treated men had significantly lower risk of acute kidney injury (HR: 0.93 [95% CI 0.87–0.98], p = 0.01) and kidney failure with replacement therapy (HR: 0.81 [95% CI 0.72–0.92], p = 0.001) compared to untreated men. Testosterone therapy was also associated with reduced risk of myocardial infarction (HR: 0.85 [95% CI 0.78–0.93], p 0.0001), ischemic stroke (HR: 0.88 [95% CI 0.80–0.97], p = 0.01), atrial fibrillation (HR: 0.91 [95% CI 0.85–0.98], p = 0.01), and all-cause mortality (HR: 0.85 [95% CI 0.79–0.91], p 0.0001).

Inositol Requiring Enzyme 1α Mediates Hypertension and Vascular Remodeling

A single genetic “switch” may be the secret to how the body’s cleanup crew grows up and keeps our organs running smoothly.

Scientists at the University of Liège have identified a crucial genetic regulator that allows macrophages to fully mature and help maintain healthy organs. This regulator, known as MafB, acts as a “molecular switch” that turns specific genes on or off at the right time and in the right cells.

By carefully controlling this genetic activity, MafB enables the development of macrophages that defend the body and support normal organ function. When MafB is missing, macrophages do not work as they should and lose their ability to carry out their protective duties.

/* */