Resumo Acacia modesta (AM) e Opuntia monocantha (OM) estão distribuídas no Paquistão, Afeganistão e Índia. Ambas as plantas têm propriedades farmacológicas diferentes. Este estudo foi desenhado para avaliar o potencial anticancerígeno de Acacia modesta (AM) e Opuntia monocantha (OM). A linha celular de câncer de fígado HepG2 foi usada para avaliação da atividade anticâncer. Para a avaliação dos efeitos antiproliferativos, a viabilidade celular e a morte celular em todos os grupos de células foram avaliadas através dos ensaios de MTT, cristal violeta e azul de tripano. Para a avaliação da apoptose foi realizado ELISA de p53. Além disso, o ensaio de LDH para descobrir a capacidade das células malignas de metabolizar o piruvato em lactato e a atividade das enzimas antioxidantes (GSH, CAT e SOD) no final da HPLC foi realizado para encontrar o composto ativo de AM e OM. Citotoxicidade (MTT), ensaios de viabilidade (azul de tripano, viabilidade de cristal, análise MUSE) mostraram mais células mortas e menos células vivas nos grupos tratados com plantas com aumento da concentração. O ensaio de arranhão para o efeito anti-migratório dessas plantas mostrou que os grupos tratados não têm capacidade de cicatrizar arranhão/ferida. ELISA de p53 para apoptose celular mostrou maior liberação de p53 nos grupos tratados. Ensaio antioxidante via glutationa (GSH), superóxido dismutase (SOD), catalase (CAT) mostrou menor potencial antioxidante nos grupos de câncer tratados. O ensaio de LDH mostrou mais liberação de lactato desidrogenase nos grupos tratados em comparação com os não tratados. A análise de HPLC mostrou a presença de fitoquímicos como esteróides, alcalóides, fenóis, flavonóides, saponinas, taninos, antraquinona e aminoácidos nos extratos vegetais AM e OM. Com base em todos esses achados, pode-se concluir que os extratos etanólicos de Acacia modesta e Opuntia monocantha apresentam potencial anticancerígeno promissor.

Abstract Acacia modesta (AM) and Opuntia monocantha (OM) are distributed in Pakistan, Afghanistan and India. Both of these plants have different pharmacological properties. This study was designed to evaluate anticancer potential of Acacia modesta (AM) and Opuntia monocantha (OM). Liver cancer cell line HepG2 was used for assessment of anticancer activity. For the evaluation of anti-proliferative effects, cell viability and cell death in all groups of cells were evaluated via MTT, crystal violet and trypan blue assays. For the evaluation of apoptosis ELISA of p53 performed. Furthermore, LDH assay to find out the ability of malignant cells to metabolize pyruvate to lactate and antioxidant enzymes activity (GSH, CAT and SOD) at the end HPLC was performed to find active compound of AM and OM. Cytotoxicity (MTT), Viability assays (trypan blue, crystal viability, MUSE analysis) showed more dead, less live cells in plant treated groups with increase of concentration. Scratch assay for the anti-migratory effect of these plants showed treated groups have not ability to heal scratch/wound. ELISA of p53 for cellular apoptosis showed more release of p53 in treated groups. Antioxidant assay via glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) showed less anti-oxidative potential in treated cancer groups. LDH assay showed more lactate dehydrogenase release in treated groups compared with untreated. HPLC analysis showed the presence of phytochemicals such as steroids, alkaloids, phenols, flavonoids, saponins, tannins, anthraquinone and amino acids in AM and OM plant extracts. Based on all these findings, it can be concluded that ethanolic extracts of Acacia modesta and Opuntia monocantha have promising anti-cancer potential.

In this work, cellulose-based composite biofilms doped with silver nanoparticles (AgNPs) have been produced by eco-friendly process. The AgNPs were synthesized from Ilex paraguariensis with an average size of 45 nm, a characteristic plasmon band at 450 nm and zeta potential of -23 mV. The biofilm has been synthesized by casting method, using different volumes of AgNPs suspension with glycerol plasticizing agent (T6-T10) or not (T1-T5). The AgNPs were successfully incorporated into the biofilms, which was confirmed by scanning electron microscopy. The mechanical and optical structural and the antimicrobial properties of the biofilms have been determined. In the presence of AgNPs, the mechanical properties, thermal stability and water vapor barrier of the biofilms have not been altered. However, the addition of glycerol decreased the tensile strength and the modulus of elasticity, in addition to increasing the elongation of the biofilms and the water vapor barrier. The biofilm T10 showed a transmittance of ca. 10%, with high potential to be used as a UV light blocker. Finally, the biofilms doped with AgNPs showed activity against the bacterium Pseudomonas fluorescens. Given the above, this work presented a new biofilm with activity against the bacterium Pseudomonus fluorescens obtained by eco-friendly process.

Abstract Leigh syndrome is an early onset progressive disorder caused by defects in mitochondrial oxidative phosphorylation. Pathogenic variants in nuclear and mitochondrial genes are associated with the syndrome. Homozygous pathogenic variants in the C12orf65 gene impair the mitochondrial oxidative phosphorylation system. We describe a new case of Leigh syndrome caused by a novel pathogenic variant of the C12orf65 gene resulting in the lack of the Gly-Gly-Gln (GGQ) domain in the predicted protein, and review clinical and molecular data from previously reported patients. Our study supports that the phenotype caused by C12orf65 gene variants is heterogeneous and varies from spastic paraparesis to Leigh syndrome. Loss-of-function variants are more likely to cause the disease, and variants affecting the GGQ domain tend to be associated with more severe phenotypes, reinforcing a possible genotype-phenotype correlation.

O efeito do estado glicêmico sobre o desenvolvimento do status epilepticus (SE) foi estudado em animais de diferentes idades, submetidos ao modelo de epilepsia por pilocarpina. Grupos: I- Ratos com nove dias (P9): IA- Submetidos a 1SE; IB- Tratados com salina; IC- Hiperglicemia induzida; ID- Hiperglicemia induzida+SE; II- Ratos submetidos a 3 episódios consecutivos de SE em P7, P8 e P9; III- Ratos submetidos a 1SE em P17; IV- Ratos submetidos a 1SE em P21. Foram analisados no grupo I a morte celular hipocampal e a expressão do transportador de glicose GLUT3. Os resultados mostraram haver normoglicemia nos grupos IA, IB e II, hipoglicemia no grupo III e hiperglicemia no grupo IV, sendo a glicemia durante o SE, idade dependente. A hiperglicemia induzida durante o SE em P9 protegeu neurônios hipocampais e os grupos IC e ID apresentaram expressão aumentada de GLUT3, mostrando aumento no consumo de glicose pelo hipocampo.

The effect of glycemic state on status epilepticus (SE) development was studied in animals of different ages, submitted to pilocarpine model of epilepsy. Groups: I- Rats with 9-day-old (P9): IA. Submitted to 1SE; IB. Saline-treated; IC. Induced- hyperglycemia; ID. Induced- hyperglycemia+SE; II- Rats submitted to three consecutive episodes of SE at P7, P8 and P9; III- Rats submitted to 1SE at P17; IV- Rats submitted to 1SE at P21. Hippocampal cell death and the expression of glucose transporter GLUT3 were analyzed in group I. The results demonstrated normoglycemia in the groups IA, IB and II, hypoglycemia in group III and hyperglycemia in group IV, showing that the glycemia during SE is age dependent. Induced hyperglycemia during SE in P9 protected the hippocampal neurons from death and both groups IC and ID presented increased GLUT3 expression, showing high glucose consumption by the hippocampus.