Pilot Study of a New Mandibular Advancement Device

This study was conducted to determine the efficacy of a customized mandibular advancement device (MAD) in the treatment of obstructive sleep apnea (OSA). Eight patients (M = 3; F = 5; mean age = 56.3 ± 9.4) with a diagnosis of OSA confirmed by polysomnography (PSG) were recruited on the basis of the following inclusion criteria: apnea-hypopnea index (AHI) > 5, age between 18 and 75 years, body mass index (BMI) < 25, and PSG data available at baseline (T0). All were treated with the new NOA® MAD by OrthoApnea (NOA®) for at least 3 months; PSG with NOA in situ was performed after 3 months of treatment (T1). The following parameters were calculated at T0 and T1: AHI, supine AHI, oxygen desaturation index (ODI), percentage of recording time spent with oxygen saturation <90% (SpO2 < 90%), and mean oxygen desaturation (MeanSpO2%). Data were submitted for statistical analysis. The baseline values were AHI = 21.33 ± 14.79, supine AHI = 35.64 ± 12.80, ODI = 17.51 ± 13.5, SpO2 < 90% = 7.82 ± 17.08, and MeanSpO2% = 93.45 ± 1.86. Four patients had mild OSA (5 > AHI < 15), one moderate OSA (15 > AHI < 30), and three severe OSA (AHI > 30). After treatment with NOA®, statistically significant improvements in AHI (8.6 ± 4.21) and supine AHI (11.21 ± 7.26) were recorded. OrthoApnea NOA® could be an effective alternative in the treatment of OSA: the device improved the PSG parameters assessed

DataSheet1_Neurodegeneration: can metabolites from Eremurus persicus help?.docx

The number of patients affected by neurodegenerative diseases is increasing worldwide, and no effective treatments have been developed yet. Although precision medicine could represent a powerful tool, it remains a challenge due to the high variability among patients. To identify molecules acting with innovative mechanisms of action, we performed a computational investigation using SAFAN technology, focusing specifically on HuD. This target belongs to the human embryonic lethal abnormal visual-like (ELAV) proteins and plays a key role in neuronal plasticity and differentiation. The results highlighted that the molecule able to bind the selected target was (R)-aloesaponol-III-8-methyl ether [(R)-ASME], a metabolite extracted from Eremurus persicus. Notably, this molecule is a TNF-α inhibitor, a cytokine involved in neuroinflammation. To obtain a suitable amount of (R)-ASME to confirm its activity on HuD, we optimized the extraction procedure. Together with ASME, another related metabolite, germichrysone, was isolated. Both ASME and germichrysone underwent biological investigation, but only ASME confirmed its ability to bind HuD. Given the multifactorial nature of neurodegenerative diseases, we decided to investigate ASME as a proteasome activator, being molecules endowed with this kind of activity potentially able to counteract aggregations of dysregulated proteins. ASME was able to activate the considered target both in enzymatic and cellular assays. Therefore, ASME may be considered a promising hit in the fight against neurodegenerative diseases.</p