All biogels are heterogeneous, consisting of functional groups with different biophysical properties arrayed on spatially disordered polymer networks. Nanoparticles diffusing in such biogels experience a mixture of attractive and repulsive interactions. Here, we present experimental and theoretical studies of charged particle diffusion in gels with a random distribution of attractive and repulsive electrostatic interaction sites inside the gel. In addition to interaction disorder, we theoretically investigate the effect of spatial disorder of the polymer network. Our coarse-grained simulations reveal that attractive interactions primarily determine the diffusive behavior of the particles in systems with mixed attractive and repulsive interactions. As a consequence, charged particles of either sign are immobilized in mixed cationic/anionic gels because they are trapped near oppositely charged interaction sites, whereas neutral particles diffuse rapidly. Even small fractions of oppositely charged interaction sites lead to strong trapping of a charged particle. Translational diffusion coefficients of charged probe molecules in gels consisting of mixed cationic and anionic dextran polymers are determined by fluorescence correlation spectroscopy and quantitatively confirm our theoretical predictions.

Patient: Male, 28-year-old Final Diagnosis: Alcohol intoxication • Brugada pattern • diabetic ketoacidosis • hyperkalemia Symptoms: Encephalopathy Medication:— Clinical Procedure: — Specialty: Cardiology Objective: Rare disease Background: Brugada syndrome is a rare ion channelopathy that can lead to sudden cardiac death and lethal arrhythmias in patients without a structural cardiac defect, the most common of which being the gain-of-function mutation of the SCN5a sodium ion channel involving phase 0 of the cardiac action potential. In 2012, BrS electrocardiogram findings were redefined and classified as either congenital Brugada syndrome (BrS) or Brugada pheno-copies (BrP). Several etiologies of BrP have been reported, such as metabolic derangements, electrolyte abnormalities, cardiovascular diseases, and pulmonary embolism. Case Report: A 28-year-old man presented to the Emergency Department unresponsive. An initial ECG taken by Emergency Medical Services (EMS) was interpreted as a STEMI. An initial ECG in the ED showed a Brugada type I ECG pattern in leads V1-V2 and hyperacute T wave abnormalities, among other findings. Additionally, the patient had a serum potassium level of 9 mmol/L, glucose level of 1375 mmol/L, and peak cardiac troponin-I of 20.452 μg/L. All underlying medical conditions were stabilized, electrolyte and metabolic abnormalities were corrected, and subsequent normalization of electrocardiographic findings was achieved. Conclusions: Distinguishing congenital Brugada syndrome from Brugada phenocopies can be difficult, especially when patients present to the ED with severe underlying conditions. Several factors can be used to direct clinical suspicion towards one or the other; however, confirmation may require EP studies and further tests. In this case, the following findings were suggestive of BrP: presence of an identifiable underlying abnormality, correction of the underlying condition resolves the ECG pattern, and the absence of family history of sudden cardiac death.

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