Myofibrillar protein microgel particles (MMP) are promising Pickering stabilisers due to their structure and delivery potential. However, their fibrous, irregular shape promotes aggregation, limiting practical use. This study investigated the effect of xanthan gum (XG) concentration (0.025–0.4%) on MMP dispersion in water and its role in stabilising Pickering emulsions. FTIR and interaction analysis revealed that hydrophobic interactions dominate between XG and MMP, followed by hydrogen bonding and electrostatic forces. At higher XG concentrations (0.2–0.4%), complex particle size decreased from 5.21 μm to 4.49 μm, the contact angle increased from 57.67° to 77.33°, and a uniform dispersed state was achieved. Although increasing XG gradually reduced the emulsifying activity of MMP, it significantly improved the emulsion stability. Microstructure analysis showed that at low XG concentrations, emulsions exhibited phase separation. Rheological measurements indicated that XG-MMP complexes increased continuous-phase viscosity and shear resistance, enhancing macroscopic stability. In summary, at a critical XG concentration of 0.2%, the emulsion undergoes a transition from aggregation-driven instability to network-mediated stabilisation, achieved through the interfacial layer with spatial confinement by a weak aqueous-phase network. This work provides a theoretical foundation and a practical design strategy for fabricating highly stable, tuneable Pickering emulsions based on protein microgel particles.

Background/Objectives: Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder driven by mutations in the NF1 gene, whose pathogenesis centers on the loss of neurofibromin function and subsequent hyperactivation of the RAS/MAPK pathway. Notably, to the best of our knowledge and following a systematic literature search conducted by our research team, no cases of NF1 complicated by severe cardiac structural abnormalities that ultimately lead to cerebral infarction have been reported to date. Thus, it is of paramount importance to avoid missed diagnosis by performing comprehensive cardiac-related examinations in patients with NF1. Case Presentation: A 20-year-old male patient diagnosed with NF1 presented with right-sided limb weakness and was initially identified with cerebral infarction. To clarify the underlying etiology, a comprehensive clinical evaluation was performed, including cardiac imaging assessments (to characterize cardiac structural changes) and whole-exome sequencing (to identify the presence of procoagulant gene mutations). Comprehensive evaluation revealed a spectrum of cardiac structural abnormalities in the patient: aortic valve prolapse with severe regurgitation, non-infective vegetations on the aortic valve leaflets, mild-to-moderate mitral regurgitation, left ventricular hypertrophy and dilation, and left atrial dilation. Whole-exome sequencing detected exclusively a pathogenic variant in the NF1 gene, with no other pathogenic/likely pathogenic variants or thrombophilia-associated polymorphisms being found. Laboratory investigations ruled out infectious etiologies, supporting the notion that NF1-mediated cardiac structural and developmental anomalies are the primary driver of cardiac vegetation formation, given the absence of other identified contributing factors; embolization of one such vegetation ultimately led to both splenic and cerebral infarction. Conclusions: This case emphasizes the necessity of implementing early and proactive cardiac evaluations in patients with NF1. Additionally, for NF1 individuals—particularly those presenting with suggestive vascular or cardiac symptoms—a comprehensive multifactorial assessment of thrombotic risk is critical. Collectively, maintaining clinical vigilance for cardiac abnormalities in NF1 patients and avoiding diagnostic oversight is essential to reduce life-threatening risks.