Abstract: Passive acoustic monitoring (PAM) is a non-invasive technique to supervise the wildlife. Acoustic surveillance is preferable in some situation such as in the case of marine mammals, when the animals spend most of their time underwater, making it hard to obtain their images. Machine learning is very useful for PAM, for example, to identify species based on audio recordings. But some care should be taken to evaluate the capability of a system. We define PAM-filters as the creation of the experimental protocols according to the dates and locations of the recordings, aiming to avoid the use of the same individuals, noise and recording devices in both training and test sets. A random division of a database present accuracies much higher than accuracies obtained with protocols generated with PAM-filter. Although we use the animal vocalizations, in our method we convert the audio into spectrogram images, after that, we describe the images using the texture. Those are well-known techniques for audio classification, and they have already been used for species classification. Also, we perform statistical tests to demonstrate the significant difference between accuracies generated with and without PAM-filters with several well-known classifiers. The configuration of our experimental protocols and the database were made available online.

Metabolic dysfunction associated fatty liver disease (MAFLD) has gained worldwide attention as a public health problem. Nonetheless, lack of enough mechanistic knowledge restrains effective treatments. It is known that T3 regulate hepatic lipid metabolism, and mitochondrial function. Liver dysfunction of T3 contributes to MAFLD, but its role is not fully understood. Objective: To evaluate the role of T3 dysfunction in the progression of MAFLD in an animal model. Method-ology: Male/adult Sprague Dawley rats (n=20) were allocated to a control group (standard di-et–2.93kcal/g) and diet group (CDHF–4.3kcal/g). Euthanasia took place in the 28th week. D3 ac-tivity and expression, UCP2 and D1 expression, REDOX status, mitochondrial, Krebs cycle and endoplasmic reticulum homeostasis in liver tissue were measured. Results: We observed an in-crease in D3 activity/expression (P<0.001) related to increased TBARS and carbonyls and GSH reduction in the MAFLD group (P<0.05). There was a T3-dependent decrease in UCP2 expression (P=0.01), mitochondrial capacity, respiratory activity with increased endoplasmic reticulum stress in the MAFLD group (P < 0.001). Surprisingly, in and environment with lower T3 levels we observed an augmented alpha-ketoglutarate dehydrogenase (KGDH) and glutamate dehydro-genase (GDH) enzymes activity (P<0.05). Conclusion: Induced D3, triggered by changes in the REDOX state, decreases T3 availability, and hepatic mitochondrial capacity. The Krebs cycle en-zymes were altered as well as reticulum stress. Taken together, these results shed new light on the role of T3 metabolism in MAFLD and new treatment opportunities.