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Senate health panel delays vote on CDC nominee

WASHINGTON — The Senate’s health panel delayed until next week a vote on Erica Schwartz to run the Centers for Disease Control and Prevention, after postponing a separate vote on Sean Kaufman for a key public health preparedness role.

The committee vote on Schwartz was pushed back because too few senators showed up. Sen. Lisa Murkowski (R-Alaska) is dealing with a family emergency, and at least one other lawmaker was also absent.

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“Physical Twins” of Human Arteries Predict Individual Stroke Risk 

Scientists in Australia have developed an artery-on-a-chip platform that can replicate a patient’s exact vascular structure to better assess their risk of ischemic stroke. Results published today in Cell Biomaterials show that differences in artery shape explain significant differences in stroke risk seen between patients with similar levels of artery narrowing. 

“Our findings suggested that three-dimensional vascular shape and local flow disturbances matter far more than simple narrowing,” said Yunduo Charles Zhao, graduate student at the University of Sydney and the Heart Research Institute in Newtown, Australia. “We hope these tools will allow us to study drugs aimed at reducing the risk of stroke and to eventually provide personalized treatments for each patient based on their anatomy.” 

Despite significant advances in imaging and management, stroke risk stratification is still very imprecise. Nearly 20% of patients receiving what is considered an optimal antiplatelet therapy continue to experience recurrent strokes, reflecting an incomplete understanding on how complex mechanical and biological factors determine whether clots grow, stabilize, or cause a stroke. 

“This idea was born out of a critical clinical gap,” said Lining Arnold Ju, PhD, associate professor at the University of Sydney in Australia and senior author of the study. “We know that even patients at ‘low risk’ can suffer from severe or fatal strokes. We wanted to find a better way to predict this risk.” 

Ju’s team used high-resolution 3D printing to create a “physical twin” that replicated the three-dimensional structure of the carotid artery from six patients who had previously experienced stroke of the carotid artery. To capture the full complexity of each patient’s unique physiology, the model also included the thrombogenic matrix and endothelium tissues, and simulated blood flow through the chip. 

“Our work recreates precise, patient-specific carotid artery geometries,” said Ju. “The physical twin also uses cells that more closely mimic the dynamics of blood flow in these structures.”

Using computer simulations, the researchers modeled blood flow through each carotid artery, uncovering substantial differences in local blood flow despite similar degrees of narrowing. They then used a laser to create an injury in the physical twins and study how blood clots formed, revealing that subtle differences in an artery’s shape could lead to strikingly different clotting responses. 

The researchers are currently recruiting patients with a stroke history for a clinical trial designed to evaluate the potential of this technology to improve diagnosis and treatment in underserved stroke patients. Down the line, the artery-on-a-chip physical twins could find applications in other cardiovascular conditions, such as peripheral artery disease, deep-vein thrombosis, and aneurysms. 

 

The post “Physical Twins” of Human Arteries Predict Individual Stroke Risk  appeared first on Inside Precision Medicine.

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<![CDATA[ASCP updates spotlight ketamine safety guardrails, at‑home agitation therapy, psilocybin phase 3 momentum, and biomarker-driven precision psychiatry.]]>
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<![CDATA[Top 2026 psychiatry conference takeaways: mixed-feature bipolar care, GLP-1 addiction trials, schizophrenia adherence, TD gaps, AI prodrome screening.]]>
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<![CDATA[SIRS highlights new schizophrenia advances: LB-102 shows promise, Cobenfy switching stays stable, and tazbentetol targets synaptic regeneration.]]>
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Vagus nerve–driven microbiota homeostasis: a promising integrative add-on therapy for neurodevelopmental disorders

Over the past two decades, the conceptualization of neurodevelopmental disorders (NDDs) has undergone a profound transformation, shifting from a primarily brain-centric framework toward a systems-level perspective that integrates peripheral physiological processes. Among these, the gut microbiota has emerged as a critical determinant of neurodevelopmental trajectories. Through its involvement in immune modulation, metabolic signaling, and neural communication, the microbiota–gut–brain axis (MGBA) exerts a pervasive influence on brain maturation and function. A growing body of evidence indicates that early-life disruptions of microbiota composition—commonly referred to as dysbiosis—are associated with an increased risk of NDDs, including autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and epilepsy. These disruptions are frequently driven by environmental exposures such as antibiotic use, cesarean delivery, dietary patterns, and psychosocial stress. Despite the expanding recognition of these associations, current therapeutic strategies aimed at restoring microbiota balance, including probiotics and fecal microbiota transplantation, have yielded inconsistent and often transient results. In this context, Vagus Nerve Stimulation (VNS), particularly in its non-invasive forms (nVNS), has emerged as a promising approach capable of modulating environmental exposures through the host-centered regulatory mechanisms of the MGBA. By influencing autonomic tone, activating the cholinergic anti-inflammatory pathway, and modulating neurotransmitter systems, nVNS may restore microbiota homeostasis while simultaneously improving neurodevelopmental outcomes. This article provides a comprehensive and integrative review of the mechanistic, preclinical, and clinical evidence supporting the role of nVNS as a microbiota-modulating intervention. We further discuss its potential as a safe, cost-effective and promising therapeutic strategy for neurodevelopmental disorders, with a particular emphasis on pediatric populations.
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Catastrophic consequences of prolonged immobilization after intracerebral hemorrhage: a case report of crush syndrome combined with capillary leak syndrome

BackgroundSpontaneous intracerebral hemorrhage is a neurological emergency with high mortality and disability rates. Prolonged immobilization after stroke can trigger severe systemic complications. The simultaneous occurrence of crush syndrome and capillary leak syndrome in the setting of acute intracerebral hemorrhage is extremely rare and life-threatening, and no established treatment protocol exists.Case summaryA 64-year-old man with hypertension was found unconscious on his home floor. The estimated time from onset to discovery exceeded 24 h. He was diagnosed with left basal ganglia intracerebral hemorrhage of approximately 5.6 mL with intraventricular extension. On admission, he was comatose with a Glasgow Coma Scale score of 9. Systemic involvement was extensive: severe bilateral leg swelling with multiple tension bullae, acute kidney injury requiring continuous renal replacement therapy, severe rhabdomyolysis with a peak creatine kinase exceeding 50,000 U/L, hyperkalemia, with an initial arterial blood gas in the emergency department showing 6.9 mEq/L, elevated liver enzymes, and distributive shock. Admission central venous pressure was negative, strongly indicating severe hypovolemia. Chest CT already showed hypostatic pneumonia. The clinical presentation was consistent with crush syndrome from prolonged compression, which then led to secondary capillary leak syndrome. The patient underwent emergency neuroendoscopic hematoma evacuation and external ventricular drainage. Postoperatively, he developed atrial fibrillation and deep vein thrombosis. After 3 weeks of multidisciplinary intensive care, his liver and kidney function gradually improved, and the hypostatic pneumonia was controlled. He survived to discharge with a Glasgow Coma Scale score of 11, left limb muscle strength grade 3/5, and right limb muscle strength grade 0/5, and was transferred to a local hospital for continued rehabilitation. At 3-month follow-up, he was walking independently (mRS 2), with significant improvements in neurological function and quality of life.ConclusionThis case reveals a frequently overlooked but deadly clinical pathway: prolonged immobilization after intracerebral hemorrhage can lead to traumatic rhabdomyolysis, crush syndrome, and secondary capillary leak syndrome. A negative central venous pressure, a rare finding, provided supportive evidence of severe hypovolemia due to capillary leak syndrome. This clinical triad represents a unique high-risk condition that demands a shift in treatment philosophy from neurocentric care to systemic resuscitation.
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Delayed multiple hemorrhagic brain metastases from atrial myxoma: a case report and literature review

ObjectiveBrain metastases from atrial myxoma are rare central nervous system manifestations and may mimic hemorrhagic malignant metastases or vascular lesions. We report a delayed case after prior cardiac myxoma resection and summarize the available patient-level literature.MethodsWe retrospectively reviewed the clinical course, multimodal neuroimaging, surgical findings, histopathology, immunohistochemistry, vascular imaging, and follow-up of a woman in her early 70s. A literature review was performed using PubMed, Web of Science, Embase, and Google Scholar from inception to 19 June 2026 with search terms related to cardiac/atrial myxoma, brain/intracranial metastasis, brain metastases, implantation, and cerebral aneurysm. Cases with histologically confirmed intracranial parenchymal myxomatous lesions were included.ResultsThe patient presented with recurrent dizziness, gait instability, right-sided weakness, and incomplete homonymous hemianopia. Brain lesions were detected 5 months after surgical resection of a left atrial myxoma, and echocardiography showed no local recurrence of the cardiac tumor. Brain CT and MRI demonstrated multiple hemorrhagic enhancing lesions with perilesional edema involving the cerebellar vermis, left occipital lobe, and other cerebral and cerebellar regions. Preoperative CTA showed no suspicious intracranial aneurysm. Two representative symptomatic lesions were surgically removed because of diagnostic uncertainty and local mass effect, whereas the remaining multifocal hemorrhagic lesions were managed with close radiological surveillance. Histology showed spindle/stellate cells in abundant myxoid stroma, and immunohistochemistry was positive for calretinin and CD31 but negative for GFAP and desmin, supporting brain metastases from atrial myxoma. At 6-month follow-up, MRI showed no local recurrence and repeat CTA showed no suspicious aneurysm.ConclusionDelayed hemorrhagic brain metastases from atrial myxoma should be considered when patients with a history of cardiac myxoma develop new neurological symptoms and multiple hemorrhagic enhancing brain lesions. Diagnosis requires integration of clinical history, neuroimaging, vascular imaging, radiology-pathology correlation, and immunohistochemistry. Treatment and surveillance should be individualized because embolic stroke, myxomatous aneurysms, and parenchymal metastases may coexist and recurrence can occur after long latency.
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Intraocular pressure spikes after intravitreal injection and their impact on OCT angiography

PurposeTo evaluate whether acute intraocular pressure (IOP) elevation after intravitreal anti-VEGF injection affects superficial capillary plexus (SCP) perfusion metrics on optical coherence tomography angiography (OCTA).MethodsIn this prospective single-center study, adults scheduled for unilateral intravitreal anti-VEGF treatment for macular edema were enrolled. Assessments were performed pre-injection (T1), early post-injection (T2), and 10 min after T2 (T3). OCTA (CIRRUS HD-OCT 5000; AngioPlex Metrix v11.0) used 6 × 6 mm fovea-centered scans. SCP vessel density (VD) and perfusion density (PD) were quantified for central (1 mm), inner (3 mm), and full macular fields (ETDRS grid). IOP was measured at T1–T3. Scans with signal strength index (SSI) < 6 or relevant motion/segmentation artefacts were excluded. Spearman correlation and multivariable regression analysis assessed associations of VD/PD with IOP and SSI.ResultsOf 81 recruited subjects, 54 eyes (66.7%) finally met OCTA quality criteria at all timepoints and were analyzed. Mean IOP increased from 13.98 ± 3.09 mmHg (T1) to 31.15 ± 9.65 mmHg (T2; p < 0.0001) and decreased to 16.30 ± 4.60 mmHg at T3 (p = 0.6246 vs. T1). Full-field SCP VD and PD decreased from 15.07 ± 3.01 and 36.23 ± 7.60 (T1) to 13.76 ± 3.50 and 33.21 ± 9.08 (T2), and to 13.22 ± 2.99 and 31.73 ± 7.67 (T3). Between T1 and T2, no OCTA parameter changed significantly. At T3, all SCP parameters were significantly lower versus at T1 except for central VD (p = 0.1495) and central PD (p = 0.2894). SSI declined from 8.35 ± 1.39 (T1) to 7.72 ± 1.42 (T2; p = 0.0105) and 7.09 ± 1.38 (T3; p < 0.0001). Correlations between VD/PD and IOP were weak (rs ≤ 0.17), whereas correlations with SSI were moderate-to-strong (rs = 0.53–0.83).ConclusionIntravitreal anti-VEGF injection caused a marked acute IOP spike, but most SCP OCTA metrics did not change at T2. The decline in SCP metrics at T3 coincided with reduced SSI and correlated more strongly with image quality than with IOP, indicating that post-procedural OCTA image quality may influence measured perfusion metrics; however, in the absence of blood pressure measurements, a physiological contribution cannot be excluded.