Ethanolamine Oleate

Acyl-CoA synthetases (ACSLs) are a family of enzymes that convert intracellular fatty acids into acyl-CoA. A previous study has demonstrated that the yeast ACSL Faa1 (a homolog of mammalian ACSL4) is involved in autophagosome membrane elongation. In the present study, we investigated the involvement of ACSL3, a key enzyme responsible for lipid droplet formation, in autophagosome formation and compared its role with that of ACSL4. Knockdown of ACSL3 impaired starvation-induced autophagy concomitant with the formation of enlarged autophagosome-like structures negative for WIPI2, whereas its overexpression resulted in the formation of WIPI2-positive, but LC3-negative dots, under normal nutrition conditions, likely in an enzymatic activity-independent manner. In contrast, ACSL4 knockdown inhibited starvation-induced autophagosome formation, whereas its overexpression caused autophagosome formation under normal nutrition conditions. Inhibition of autophagosome formation in ACSL4-depleted cells could be rescued by ethanolamine, suggesting a deficit of phosphatidylethanolamine in ACSL4-depleted cells. These results suggest that ACSL3 and ACSL4 are involved in different stages of autophagosome formation - ACSL3 in the formation of fusion-competent autophagosomal membranes and ACSL4 in the formation of autophagosomes.

To describe the characteristics and outcomes of a cohort of patients with oral vascular anomalies (OVA) treated with sclerotherapy using 5% ethanolamine oleate at a dosage of 0.1 mL per 10 mm of lesion size.

Sixty-seven patients were selected from a review of 300 medical records of individuals who had been diagnosed with OVA. Clinicodemographic characteristics and treatment outcomes were analyzed descriptively and analytically.

The overall mean number of sclerotherapy sessions required for clinical healing was 1.1, with lesions up to 6 mm typically requiring only one session. The mean volume of 5% ethanolamine oleate administered was 0.1 mL; however, 97.1% of lesions up to 6 mm were successfully treated with a maximum dose of 0.05 mL. Patients with papular lesions had a significantly lower rate of clinical healing compared to those with macular lesions (OR=0.79; [0.64-0.96]; p=.021). The average time to clinical healing was 16.0 days, with lesions up to 6 mm generally healing within 14 days. Complete clinical healing was achieved in 65.7% of cases.

The low-dose sclerotherapy protocol using 5% ethanolamine oleate is effective for treating OVA, particularly for lesions measuring up to 6 mm in diameter.