Education as a Predictor Factor for Knowledge of COVID-19 in Portugal.

Introduction/Objective: Pandemic of COVID-19 is a major public health problem. At the time of development of this study, no specific medication/vaccine for this disease was approved. Therefore, preventive measures were the main key to control this pandemic. Health literacy (HL) is the ability to obtain, understand and use the information to make free and informed decisions about the health of an individual and to promote community empowerment. Thus, the HL of COVID-19 is important for community empowerment and the adoption of preventive measures. This article aims to understand possible predictors of HL of COVID-19, functional domain. Material and Methods: A cross-sectional study was designed, applying the Questionnaire of COVID-19 (previously designed and submitted to a preliminary pilot testing) through an online platform from April 23 to June 23, 2020. An Index of Health Knowledge of COVID-19 Questionnaire (IHK-COV19) was constructed. Associations between independent variables ("Gender," "Age," "Education," and "Risk Factor" for COVID-19 codified by ICPC-2) and HL were assessed using multivariate analyses (mixed effects models). The level of significance was set at p < 0.05. Results: Our sample includes 864 subjects (median age, 44.33 years), mostly women (n = 619; 71.76%), undergraduate (n = 392; 45.37%) and with at least one risk factor for COVID-19 (n = 266; 30.79%). Univariate and multivariate analyses demonstrated "Age" as a negative predictor of IHK-COV19 and "Education" and "Risk Factor" as positive predictors of IHK-COV19. Conclusions: Health knowledge regarding COVID-19 is associated with the level of education. Future interventions should consider including HL mechanisms in interventions designed to improve communication.

Say it aloud: Measuring change talk and user perceptions in an automated, technology-delivered adaptation of motivational interviewing delivered by video-counsellor.

Motivational Interviewing is a widely used counselling technique. A fundamental principle of this technique is that hearing oneself argue for change strengthens motivation. This study presents the first analysis of participants' dialogue with an automated motivational interviewer. The objective was to explore communication with, and perceptions of, a technology-delivered adaptation of motivational interviewing (TAMI) delivered by a pre-recorded video-counsellor. Eighteen participants undertook the video interview and evaluated it after one week. Interviews were scored for change and sustain talk. Participants' written evaluations were subjected to thematic analysis. Interviews lasted 10 min 30s (SD 3 min 0 s). Change talk was observed in a mean of 16 of 25 responses (SD 3.35, range 11-21). Sustain talk was less frequent (mean = 3.4 replies, SD = 2.5, range 0 to 8). Participants disliked seeing their own image in the webcam and desired a personalised interaction where each question depended on the answer given to the previous one. Positive appraisals included space to think about motivation and plans, and hearing themselves voicing goals. A brief, generic, automated TAMI elicited change talk and was perceived as motivating.

Experiences of a Motivational Interview Delivered by a Robot: Qualitative Study.

BACKGROUND: Motivational interviewing is an effective intervention for supporting behavior change but traditionally depends on face-to-face dialogue with a human counselor. This study addressed a key challenge for the goal of developing social robotic motivational interviewers: creating an interview protocol, within the constraints of current artificial intelligence, which participants will find engaging and helpful. OBJECTIVE: The aim of this study was to explore participants' qualitative experiences of a motivational interview delivered by a social robot, including their evaluation of usability of the robot during the interaction and its impact on their motivation. METHODS: NAO robots are humanoid, child-sized social robots. We programmed a NAO robot with Choregraphe software to deliver a scripted motivational interview focused on increasing physical activity. The interview was designed to be comprehensible even without an empathetic response from the robot. Robot breathing and face-tracking functions were used to give an impression of attentiveness. A total of 20 participants took part in the robot-delivered motivational interview and evaluated it after 1 week by responding to a series of written open-ended questions. Each participant was left alone to speak aloud with the robot, advancing through a series of questions by tapping the robot's head sensor. Evaluations were content-analyzed utilizing Boyatzis' steps: (1) sampling and design, (2) developing themes and codes, and (3) validating and applying the codes. RESULTS: Themes focused on interaction with the robot, motivation, change in physical activity, and overall evaluation of the intervention. Participants found the instructions clear and the navigation easy to use. Most enjoyed the interaction but also found it was restricted by the lack of individualized response from the robot. Many positively appraised the nonjudgmental aspect of the interview and how it gave space to articulate their motivation for change. Some participants felt that the intervention increased their physical activity levels. CONCLUSIONS: Social robots can achieve a fundamental objective of motivational interviewing, encouraging participants to articulate their goals and dilemmas aloud. Because they are perceived as nonjudgmental, robots may have advantages over more humanoid avatars for delivering virtual support for behavioral change.

Generation and the subjective feeling of "aha!" are independently related to learning from insight.

It has been proposed that sudden insight into the solutions of problems can enhance long-term memory for those solutions. However, the nature of insight has been operationalized differently across studies. Here, we examined two main aspects of insight problem-solving-the generation of a solution and the subjective "aha!" experience-and experimentally evaluated their respective relationships to long-term memory formation (encoding). Our results suggest that generation (generated solution vs. presented solution) and the "aha!" experience ("aha!" vs. no "aha!") are independently related to learning from insight, as well as to the emotional response towards understanding the solution during encoding. Moreover, we analyzed the relationship between generation and the "aha!" experience and two different kinds of later memory tests, direct (intentional) and indirect (incidental). Here, we found that the generation effect was larger for indirect testing, reflecting more automatic retrieval processes, while the relationship with the occurrence of an "aha!" experience was somewhat larger for direct testing. Our results suggest that both the generation of a solution and the subjective experience of "aha!" indicate processes that benefit long-term memory formation, though differently. This beneficial effect is possibly due to the intrinsic reward associated with sudden comprehension and the detection of schema-consistency, i.e., that novel information can be easily integrated into existing knowledge.

Monoamine oxidase-B mediates ecstasy-induced neurotoxic effects to adolescent rat brain mitochondria.

3,4-Methylenedioxymethamphetamine (MDMA)-induced neurotoxicity and the protective role of monoamine oxidase-B (MAO-B) inhibition were evaluated at the mitochondrial level in various regions of the adolescent rat brain. Four groups of adolescent male Wistar rats were used: (1) saline control, (2) exposed to MDMA (4 x 10 mg/kg, i.p.; two hourly), (3) treated with selegiline (2 mg/kg, i.p.) 30 min before the same dosing of MDMA, and (4) treated with selegiline (2 mg/kg, i.p.). Body temperatures were monitored throughout the whole experiment. Animals were killed 2 weeks later, and mitochondria were isolated from several brain regions. Our results showed that "binge" MDMA administration causes, along with sustained hyperthermia, long-term alterations in brain mitochondria as evidenced by increased levels of lipid peroxides and protein carbonyls. Additionally, analysis of mitochondrial DNA (mtDNA) revealed that NDI nicotinamide adenine dinucleotide phosphate dehydrogenase subunit I and NDII (nicotinamide adenine dinucleotide phosphate dehydrogenase subunit II) subunits of mitochondrial complex I and cytochrome c oxidase subunit I of complex IV suffered deletions in MDMA-exposed animals. Inhibition of MAO-B by selegiline did not reduce hyperthermia but reversed MDMA-induced effects in the oxidative stress markers, mtDNA, and related protein expression. These results indicate that monoamine oxidation by MAO-B with subsequent mitochondrial damage may be an important contributing factor for MDMA-induced neurotoxicity.

MDMA in adolescent male rats: decreased serotonin in the amygdala and behavioral effects in the elevated plus-maze test.

Long-term behavioral consequences of the neurotoxicity produced by 3,4-methylenedioxymethamphetamine (MDMA) in the adolescent rat are still mostly unknown. Here, adolescent male rats (postnatal day 45 PND [45]) were exposed to 10 mg/kg of MDMA, intraperitoneally, every 2 h for 6 h. Controls were given 0.9% saline in the same protocol. Ten days after exposure, the behavioral effects of MDMA were assessed in the elevated plus-maze (n = 6 per group). After behavioral testing, animals were sacrificed and the amygdalae were dissected and processed for HPLC determination of dopamine (DA), serotonin (5-HT), and metabolites. Results showed a significant decrease in the 5-HT content (P < 0.05), but no significant alterations in DA or its metabolites. Behavioral observation in the elevated plus-maze showed a decreased number of entries in the unprotected arms (P < 0.05), which were correlated to the number of entries and time spent in the central platform. Rearing was also decreased (P < 0.05). No differences were observed in head dips, grooming, or number of entries in the protected arms of the apparatus. Therefore, we conclude that, as in the adult rat, exposure to MDMA in the adolescent rat is associated to long-term depletion of the 5-HT content and increased anxiety-like behavior.

Effects of neonatal exposure to methamphetamine: catecholamine levels in brain areas of the developing rat.

Neonatal exposure to moderate doses of methamphetamine during the first month of life in the rat affects tyrosine hydroxylase gene expression in the substantia nigra and nigrostriatal tyrosine hydroxylase activity. The main goal of this work was to evaluate the ontogeny of the neurochemical effects of repeated exposure to moderate doses of methamphetamine during the first month of life in the rat. Norepinephrine, dopamine, and dihydroxyphenylacetic acid levels were measured in target areas of methamphetamine: the substantia nigra, ventral tegmental area, caudate-putamen, nucleus accumbens, and medial prefrontal cortex. On postnatal day 1 (PND1), Wistar rat litters, culled to eight pups, sex balanced, were randomly attributed to either methamphetamine or control groups. Methamphetamine groups were administered 10 mg of (+/-)-methamphetamine/kg body weight/day, subcutaneously, from PND1 until the day prior to sacrifice; control groups received isovolumetric saline. Groups were sacrificed on PND7, PND14, and PND30. Neonatal methamphetamine exposure increased norepinephrine levels in the substantia nigra of PND30 rats; on PND14, this variation was evident only in male pups. In the substantia nigra, the dihydroxyphenylacetic/dopamine ratio was also affected in PND30 males. In the ventral tegmental area, catecholamine levels were not affected by methamphetamine. Norepinephrine levels were also increased in the caudate-putamen of PND7 male and PND14 female methamphetamine-exposed pups and in the nucleus accumbens of PND14 female and PND30 male and female pups. Catecholamine levels in the medial prefrontal cortex were not affected by neonatal methamphetamine administration.

Genomic structure, promoter activity, and developmental expression of the mouse homologue of the Machado-Joseph disease (MJD) gene.

Machado-Joseph disease (MJD) is a neurodegenerative disorder, caused by the expansion of the (CAG)n tract in the MJD gene. This encodes the protein ataxin-3, of unknown function. The mouse Mjd gene has a structure similar to that of its human counterpart and it also contains a TATA-less promoter. Its 5' flanking region contains conserved putative binding regions for transcription factors Sp1, USF, Arnt, Max, E47, and MyoD. Upon differentiation of P19 cells, the Mjd gene promoter is preferentially activated in endodermal and mesodermal derivatives, including cardiac and skeletal myocytes; and less so in neuronal precursors. Mouse ataxin-3 is ubiquitously expressed during embryonic development and in the adult, with strong expression in regions of the CNS affected in MJD. It is particularly abundant in all types of muscle and in ciliated epithelial cells, suggesting that it may be associated with the cytoskeleton and may have an important function in cell structure and/or motility.

Prenatal exposure to methamphetamine in the rat: ontogeny of tyrosine hydroxylase mRNA expression in mesencephalic dopaminergic neurons.

Methamphetamine (Meth) is an illicit substance known to interfere with catecholaminergic systems and a popular recreational drug among young adult women, that is, in gestational age. Tyrosine hydroxylase (TH), the rate-limiting enzyme of the synthetic pathway of catecholamines, is a good marker to assess potential effects of Meth in catecholaminergic (particularly in dopaminergic) systems. In the rat, prolonged neonatal Meth exposure altered several dopaminergic markers (TH activity and gene expression) in substantia nigra pars compacta (SN) and in caudate-putamen (TH activity) when animals matured. However, it was never verified whether gestational exposure to Meth might compromise TH enzyme in the pups during the neonatal immature periods. The present study was designed to address this issue by analyzing TH gene expression, measured by in situ hybridization in SN and ventral tegmental area (VTA), dopaminergic areas that are well characterized as target areas for Meth, and in rats prenatally exposed to this psychostimulant. To this end, dated pregnant Wistar rat dams received 5 mg Meth hydrochloride/kg body weight/day. It was administered subcutaneously from gestational day 8 until 22. The control group was pair-fed and saline injected, using the same experimental protocol as for Meth-treated dams. On the day of birth (postnatal day 0, PND 0), litters were culled to 8 pups, sex-balanced whenever possible, and were followed until the day of sacrifice (PND 7, 14, or 30). Meth treatment differentially affected TH mRNA levels in VTA and SN, in an age- and gender-dependent manner. Thus, TH mRNA levels were decreased in the VTA of PND 7 and PND 14 females gestationally exposed to Meth; this effect was not evident in males or on PND 30. TH mRNA levels also tend to decrease in SN of PND 14 females gestationally exposed to Meth. Collectively, the present results indicated that gestational Meth exposure affects TH gene expression in the postnatal life, a phenomenon that appears to be transient, since it is no longer evident by the end of the first month of life in the rat.

Adaptative response of antioxidant enzymes in different areas of rat brain after repeated d-amphetamine administration.

d-Amphetamine has been shown to be a potential brain neurotoxic agent, particularly to dopaminergic neurones. Reactive oxygen species indirectly generated by this drug have been indicated as an important factor in the appearance of neuronal damage but little is known about the adaptations of brain antioxidant systems to its chronic administration. In this study, the activities of several antioxidant enzymes in different areas of rat brain were measured after repeated administration of d-amphetamine sulphate (sc, 20 mg/kg/day, for 14 days), namely glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GRed), catalase, and superoxide dismutase (SOD). When compared to a pair-fed control group, d-amphetamine treatment enhanced the activity of GST in hypothalamus to 167%, GPx in striatum to 127%, in nucleus accumbens to 192%, and in medial prefrontal cortex to 139%, GRed in hypothalamus to 139%, as well as catalase in medial prefrontal cortex to 153%. However, the same comparison revealed a decrease in the activity of GRed in medial pre-frontal cortex by 35%. Food restriction itself reduced GRed activity by 49% and enhanced catalase activity to 271% in nucleus accumbens. The modifications observed for the measured antioxidant enzymes reveal that oxidative stress probably plays a role in the deleterious effects of this drug in CNS and that, in general, the brain areas studied underwent adaptations which provided protection against the continuous administration of the drug.