Abdominal pain is a common presentation in the emergency department (ED). Ultrasound is the first-line diagnostic imaging modality for right upper quadrant pain. Point-of-care ultrasound (POCUS) is a focused examination that can be performed at the patient’s bedside to evaluate acute and emergent biliary pathology. The advantages of POCUS include avoiding the potential safety risks associated with transporting critically ill patients, no exposure to ionizing radiation, potentially reduced costs, and rapid diagnosis. This narrative review synthesizes key sonographic findings and techniques for emergent and non-emergent biliary diseases that physicians should recognize at first glance. We present significant and interesting images of cholelithiasis, acute cholecystitis, emphysematous gallbladder, choledocholithiasis or sludge, Mirizzi syndrome, post-operative biliary obstruction, gallbladder polyps, biliary neoplasms, and malignant-appearing lesions or masses. Finally, this review integrates POCUS into clinical pathways to guide decisions regarding additional abdominal imaging, such as computed tomography or radiology-performed ultrasound, and surgical consultation.

Bipolar disorder (BD) is a debilitating neuropsychiatric disorder characterized by recurrent mood perturbations, cognitive and functional impairment, and increased risk of suicide. Genome-wide association studies (GWAS) have repeatedly identified the gene ANK3 , which encodes the neuronal scaffolding protein ankyrin-G, as a risk locus for BD. Ankyrin-G interacts directly with the GABA _A receptor-associated protein (GABARAP) to stabilize inhibitory synapses, providing a potential mechanistic link between ANK3 variation and GABAergic dysfunction observed in BD. Previously, we identified an ANK3 p.W1989R variant in a family with BD and demonstrated that this variant abolishes the ankyrin-G/GABARAP interaction, resulting in inhibitory signaling deficits in mice. Here, we investigated the effects of this variant in human induced pluripotent stem cell (hiPSC)-derived neurons generated from an affected individual heterozygous for the ANK3 p.W1989R variant. CRISPR correction of the variant increased inhibitory synapse density on both glutamatergic and GABAergic patient-derived neurons. Integrated spatial transcriptomics and calcium imaging identified cell-type-dependent changes in gene expression and calcium dynamics. ANK3 p.W1989R somatostatin (SST) positive interneurons displayed altered calcium dynamics and reduced SST expression. To determine whether the variant impacts SST interneuron-mediated inhibition of cortical circuits, we selectively stimulated prefrontal cortical SST interneurons in heterozygous Ank3 p.W1989R mice and recorded optically evoked inhibitory postsynaptic currents (oIPSCs) from cortical pyramidal neurons. SST interneuron-mediated oIPSC peak amplitude, charge transfer, and decay times were reduced in variant mice, without a significant change in the paired-pulse ratio. These findings, using complementary human and mouse models, identify novel roles for ankyrin-G in SST interneuron-mediated inhibitory signaling and demonstrate that altered inhibitory connectivity and SST interneuron function are associated with ANK3 p.W1989R. This work provides mechanistic insight into how disrupted ankyrin-G-dependent synaptic function may contribute to inhibitory signaling deficits relevant to BD.