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Baru (Dipteryx alata Vogel) is recognized as a widespread Brazilian tree species, and its almonds and pulp have gained commercial prominence due to their nutritional value. All parts of the baru are important for the environment and are used by traditional communities to treat various diseases. This review provides a comprehensive and current overview of the nutritional composition, human food applications, ethnopharmacological uses, and chemical and biological properties of Dipteryx alata, "baru" (Fabaceae). This study followed the recommendations of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology. Studies were searched in the Medline (PubMed), Scopus, SciELO, and ScienceDirect databases using the descriptors "Dipteryx alata" OR "baru nut" OR "baru almond" OR "cumaru" OR "Coumarouna". The exclusion criteria included duplicate articles, review articles, case reports, short communications, conference documents, incomplete access to the text, and articles not related to the objective of this review. The initial search yielded 822 results, 127 of which met the inclusion criteria. The almond was the most extensively studied part (59.8%), whereas leaves received the least attention (1.6%). Baru almond is a rich source of proteins (19 to 30 g.100 g-1), unsaturated fatty acids (75 to 81%), and essential amino acids, while the pulp is rich in carbohydrates (22.5 to 75.4%), dietary fiber (4.4 to 41.6 g.100 g-1) and vitamin C (113.48 and 224.5 mg.100 g-1). Phenolic compounds were the main metabolites, with a greater content in the almond (3.1 to 1.306,34 mg GAE g-1) than in the pulp (186 to 477 mg GAE g-1). Terpenes were also detected in the almond, pulp, and bark. The most evaluated biological activity was the antioxidant activity (n = 32.1%), followed by effects on oxidative stress (n = 12.5%). Therefore, emphasis on baru cultivation and bioprospecting could benefit human nutrition and health, strengthen family farming in various regions of the country and favour the achievement of Zero Hunger and Sustainable Agriculture and Health and Well-Being in the UN 2030 Agenda for Sustainable Development Goals.

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This article reports the first occurrence of Rhytidodes gelatinosus (Rudolphi, 1819) Looss, 1901 (Digenea: Rhytidodidae) in the olive-ridley turtle Lepidochelys olivacea (Testudines: Chelonidae), in an individual found in the State of Sergipe, Brazil. Although R. gelatinosus has already been described in other species of sea turtles in the world, this is the first report of this parasite in L. olivacea. We also present a list of hosts and locations where this helminth has already been identified.

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BACKGROUND AND AIMS: Apolipoprotein B plays a crucial role in regulating plasma cholesterol by mediating the interaction of low-density lipoprotein (LDL) with LDL receptors in the liver. Inherited mutations in this gene may increase the risk of developing premature atherosclerotic cardiovascular disease, especially in individuals with familial hypercholesterolemia type 2 (FH2). The aim of this study is to identify APOB variants that may indicate pathogenicity in a sample of the Brazilian population using a data bank exome sequencing study by NGS in a Brazilian population phenotypically diagnosed by clinical and laboratory profile. This finding is going to improve genetic hypercholesteremia diagnosis. METHODS: High-quality DNA samples (n»300) were sequenced using an exon-targeted gene sequencing (ETGS) strategy to identify variants in FHrelated genes. Pathogenicity classification was based on criteria established by the American College of Medical Genetics and Genomics (ACMG), also using information from ClinVar and pathogenicity scores from previous association studies. RESULTS: A total of 121 variants were identified in APOB, of which four are novel variants missense (p.Thr626Asn, p.Ile2750Thr, p.Gln2078Lys and p.Met4184Arg). After curating pathogenicity scores, variants were classified according to the ACMG criteria. Among them four as pathogenic or likely pathogenic (p.Pro2739Leu, p.His1923Arg, p.Pro994Leu and p.Pro877Leu), and 21 variants had uncertain significance. Additionally, 92 previously known variants with uncertain significance were classified as benign or likely benign. The results were submitted to Clinvar for actualization of pathogenicity. CONCLUSIONS: These results improve the molecular diagnosis associating APOB variants with the clinical phenotype of hypercholesterolemia.

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Brain glucose hypometabolism and neuroinflammation are early pathogenic manifestations in neurological disorders. Neuroinflammation may also disrupt leptin signaling, an adipokine that centrally regulates appetite and energy balance by acting on the hypothalamus and exerting neuroprotection in the hippocampus. The Goto-Kakizaki (GK) rat is a non-obese type 2 diabetes mellitus (T2DM) animal model used to investigate diabetes-associated molecular mechanisms without obesity jeopardizing effects. Wistar and GK rats received the maintenance adult rodent diet. Also, an additional control group of Wistar rats received a high-fat and high-sugar diet (HFHS) provided by free consumption of condensed milk. All diets and water were provided ad libitum for eight weeks. Brain glucose uptake was evaluated by 2-deoxy-2-[fluorine-18] fluoro-D-glucose under basal (saline administration) or stimulated (CL316,243, a selective ß3-AR agonist) conditions. The animals were fasted for 10-12 h, anesthetized, and euthanized. The brain was quickly dissected, and the hippocampal area was sectioned and stored at -80°C in different tubes for protein and RNA analyses on the same animal. GK rats exhibited attenuated brain glucose uptake compared to Wistar animals and the HFHS group under basal conditions. Also, the hippocampus of GK rats displayed upregulated leptin receptor, IL-1ß, and IL-6 gene expression and IL-1ß and the subunit of the transcription factor NF-κB (p-p65) protein expression. No significant alterations were detected in the hippocampus of HFHS rats. Our data indicated that a genetic predisposition to T2DM has significant brain deteriorating features, including brain glucose hypometabolism, neuroinflammation, and leptin signaling disruption in the hippocampal area.

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OBJECTIVE: This study aimed to evaluate the effect of activated charcoal toothpaste on the color stability of teeth subjected to tooth bleaching and pigmenting agents. METHODS: A total of 120 bovine crowns were randomly divided into 12 groups (n=10) according to two study factors: staining solutions (three levels): saliva (control), coffee, and red wine; and toothpaste (four levels): BPC, Bianco Pro Clinical (Bianco Oral Care) (Control); BIW, Black is White (Curaprox); BCA, Bianco Carbon (Bianco Oral Care); and NAT, Natural Suavetex (Suavetex). The samples were subjected to office bleaching with a 35% hydrogen peroxide-based gel (Whiteness HP Blue, FGM), followed by immersion in the solution for 45 minutes per day and daily toothbrushing for 7 days. The color (ΔE) and luminosity changes (ΔL*) were measured using reflectance spectroscopy (Vita EasyShade). The CIE values (L*, a*, b*) were measured at baseline after bleaching (T0) and immediately after immersion in solution each day (Ti1-Ti7) and after all toothbrushing cycles (Tb1-Tb7). ΔE and ΔL were analyzed using a two-way analysis of variance and Tukey's test (α=0.05). The clinically unacceptable level of ΔE > 3.3 was used to evaluate the color change. RESULTS: The color change was significantly influenced by the staining solutions and toothpastes (p<0.001). The color change (ΔE) was significantly higher when immersed in wine than in coffee, and lower ΔE values were observed for artificial saliva (control), irrespective of the toothpaste used. In artificial saliva, BPC, BIW, and BCA resulted in significantly lower ΔE values than NAT, which presented a clinically unacceptable level of dental color change (ΔE>3.3). Coffee resulted in a lower (L*) reduction than wine, irrespective of the toothpaste used. CONCLUSION: Charcoal toothpastes resulted in a color change on the surface of the tooth enamel (ΔE). The bleaching effect of the charcoal toothpastes and control evaluated in this study partially reduced the color changes on the surface of the tooth enamel caused by staining solutions but was unable to reestablish the measured values to the baseline. For teeth immersed in artificial saliva, the color change was not noticeable in BCA, BIW, and control-BPC (ΔE≥3.3), except for NAT, which showed a significant color change.

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Brain glucose hypometabolism and neuroinflammation are early pathogenic manifestations in neurological disorders. Neuroinflammation may also disrupt leptin signaling, an adipokine that centrally regulates appetite and energy balance by acting on the hypothalamus and exerting neuroprotection in the hippocampus. The Goto-Kakizaki (GK) rat is a non-obese type 2 diabetes mellitus (T2DM) animal model used to investigate diabetes-associated molecular mechanisms without obesity jeopardizing effects. Wistar and GK rats received the maintenance adult rodent diet. Also, an additional control group of Wistar rats received a high-fat and high-sugar diet (HFHS) provided by free consumption of condensed milk. All diets and water were provided ad libitum for eight weeks. Brain glucose uptake was evaluated by 2-deoxy-2-[fluorine-18] fluoro-D-glucose under basal (saline administration) or stimulated (CL316,243, a selective β3-AR agonist) conditions. The animals were fasted for 10-12 h, anesthetized, and euthanized. The brain was quickly dissected, and the hippocampal area was sectioned and stored at -80°C in different tubes for protein and RNA analyses on the same animal. GK rats exhibited attenuated brain glucose uptake compared to Wistar animals and the HFHS group under basal conditions. Also, the hippocampus of GK rats displayed upregulated leptin receptor, IL-1β, and IL-6 gene expression and IL-1β and the subunit of the transcription factor NF-κB (p-p65) protein expression. No significant alterations were detected in the hippocampus of HFHS rats. Our data indicated that a genetic predisposition to T2DM has significant brain deteriorating features, including brain glucose hypometabolism, neuroinflammation, and leptin signaling disruption in the hippocampal area.

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Brain glucose hypometabolism and neuroinflammation are early pathogenic manifestations in neurological disorders. Neuroinflammation may also disrupt leptin signaling, an adipokine that centrally regulates appetite and energy balance by acting on the hypothalamus and exerting neuroprotection in the hippocampus. The Goto-Kakizaki (GK) rat is a non-obese type 2 diabetes mellitus (T2DM) animal model used to investigate diabetes-associated molecular mechanisms without obesity jeopardizing effects. Wistar and GK rats received the maintenance adult rodent diet. Also, an additional control group of Wistar rats received a high-fat and high-sugar diet (HFHS) provided by free consumption of condensed milk. All diets and water were provided ad libitum for eight weeks. Brain glucose uptake was evaluated by 2-deoxy-2-[fluorine-18] fluoro-D-glucose under basal (saline administration) or stimulated (CL316,243, a selective β3-AR agonist) conditions. The animals were fasted for 10-12 h, anesthetized, and euthanized. The brain was quickly dissected, and the hippocampal area was sectioned and stored at -80°C in different tubes for protein and RNA analyses on the same animal. GK rats exhibited attenuated brain glucose uptake compared to Wistar animals and the HFHS group under basal conditions. Also, the hippocampus of GK rats displayed upregulated leptin receptor, IL-1β, and IL-6 gene expression and IL-1β and the subunit of the transcription factor NF-κB (p-p65) protein expression. No significant alterations were detected in the hippocampus of HFHS rats. Our data indicated that a genetic predisposition to T2DM has significant brain deteriorating features, including brain glucose hypometabolism, neuroinflammation, and leptin signaling disruption in the hippocampal area.

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Background and Aim: New substances for neoplasm treatment have to be carefully studied to minimize adverse effects and prevent disease progression stimulation. Jatobá is a typical tree of the Cerrado and Caatinga biome, with antifungal, antimicrobial, larvicide, antioxidant, and antiproliferative properties. This study aimed to investigate the action of the crude extract of Jatobá leaves (EBFJ) on canine osteosarcoma (CO) cells and analyze the expression of biomarkers in neoplasm progression. Materials and Methods: D17 cells were cultured and subjected to treatment with EBFJ at different concentrations (10 µg/mL; 100 µg/mL; 1000 µg/mL; 2000 µg/mL; and 5000 µg/mL) and exposure times (24 h, 48 h, and 72 h). The tetrazolium reduction assay and the immunocytochemistry technique, with anti-Bcl2, anti-p53, and anti-Ki-67 antibodies, were used to observe the effect of the extract on cell proliferation. Results: Doses of 2000 µg and 5000 µg had cell viability of 300.80% and 361.84%, respectively. The extract did not show significant cytotoxicity of samples with the control group. The confluence of cells, the number of labeled cells, and the expression of Bcl2, Ki-67, and p53 were higher in the groups treated with EBFJ, with a statistical difference from the group without treatment. Conclusion: EBFJ was not cytotoxic and had a proliferative effect on CO D17 cells. The confluence of cells, the number of labeled cells, and the expression of Bcl2, Ki-67, and p53 were higher in the groups treated with the extract.

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OBJECTIVE: This study was designed to evaluate the effects of charcoal toothpaste on the surface roughness, color stability, and marginal staining of resin composite restorations. METHODS: A total of 100 bovine incisors was collected. The crowns were sectioned and randomly divided into 10 groups (n=10) according to two study factors: toothpaste groups and nanoparticle resin composite groups. Five toothpastes-Bianco Pro Clinical (Bianco Oral Care, Uberlândia, MG, Brazil) - Control group; Bianco Carbon (Bianco Oral Care); NAT, Natural Suavetex Carvão Ativado (Suavetex, Uberlândia, MG, Brazil); Nano Action Black Be Emotion (Polishop, Jundiaí, SP, Brazil); and BIW, Black is White (Curaprox, Curaden AG, Kriens, Switzerland)-and two resin composites-Z350XT (Filtek Z350XT, 3M Oral Care) and Vittra (Vittra APS FGM, Joinville, SC, Brazil)-were used. Circular cavities with a diameter of 4 mm and a depth of 1 mm were prepared on the buccal face of the tooth crowns and restored with resin composites. The specimens were subjected to three months of simulated toothbrushing. The surface roughness (right angle [Ra], in micrometers [µm]) of the resin composites was measured before and after toothbrushing in five areas per specimen. The resin composite color and luminosity changes (ΔE and ΔL, respectively) were measured using reflectance spectroscopy (Vita EasyShade). Macro photographs were taken before and after toothbrushing to qualitatively analyze the marginal staining (MSt) of the resin composite restorations. Scanning electron microscopy (SEM) was performed before and after the simulated toothbrushing. Ra data were analyzed using two-way analysis of variance with repeated measures and the Tukey HSD test; MSt was analyzed using Kruskal-Wallis and Dunn tests (α=0.05), and the resin composite color change was analyzed using the clinically unacceptable level of ΔE > 3.3. RESULTS: Simulated brushing increased Ra irrespective of the resin composite or toothpaste used. No significant differences were found in Ra between the control group and all groups on which the charcoal toothpastes were tested. A clinically unacceptable level of resin composite color change (ΔE>3.3) was found after the use of most charcoal toothpastes. Use of Bianco Carbon resulted in marginal staining similar to that of the control group and was lower than that of the other charcoal toothpastes. Vittra brushed with black toothpaste showed the highest marginal staining. CONCLUSION: Use of charcoal toothpaste resulted in Ra values of resin composites similar to those found with conventional toothpastes. Charcoal toothpaste generally resulted in clinical resin composite color changes (ΔE). All charcoal toothpastes, except Bianco Carbon, caused marginal staining of the resin composite restorations.

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INTRODUÇÃO: A hipercolesterolemia familiar (HF) é uma doença hereditária autossômica codominante marcada por altos níveis de colesterol ligado à lipoproteína de baixa densidade (LDL-c). Pode-se apresentar na forma homozigótica, apresentando prevalência de 1/160.000 a 1/1.000.000 ou na forma heterozigótica, um caso em cada 200-250 pessoas. Material e MÉTODO: Paciente do sexo feminino, aos 11 meses foi encaminhada ao setor de Dislipidemia para acompanhamento. Na primeira consulta, apresentava colesterol total (CT): 325 mg/dL, LDL-c: 255 mg/dL, colesterol ligado à lipoproteína de alta densidade (HDL-c): 44 mg/dL, triglicerídeos (TG): 128 mg/ dL. Exame físico: sem alterações. Durante o seguimento, paciente realizou doppler de carótidas e vertebrais sem aumento da espessura médio intimal e tomografia computadorizada com escore de cálcio de zero. Paciente foi incluída no protocolo para o sequenciamento exômico dos principais genes relacionados com a HF. A paciente apresentou 9 diferentes variantes, todos em heterozigose, com cobertura maior que 30 vezes, distribuídas nos 3 genes, no entanto nenhuma previamente associada com HF. RESULTADOS: Trata-se de uma criança cuja alteração do perfil lipídico foi identificada precocemente. A análise do perfil genético identificou uma mutação que está relacionada ao fenótico de HF. As variantes mais comuns relacionadas à HF estão localizadas no gene que codifica o receptor da LDL (LDLR). Dentre as variantes analisadas, somente a variante rs1433099 no gene LDLR foi previamente associada a elevação do LDL-c e maior suscetibilidade a desenvolver doença arterial coronariana. No entanto esse achado nunca havia sido descrito em pacientes com diagnóstico clínico de HF. DISCUSSÃO E CONCLUSÕES: O relato de caso apresentou uma variante genética que não havia sido descrita previamente relacionada à HF. Dessa forma, devido à grande importância da hereditariedade nos quadros de dislipidemias, à pequena parcela de genes descritos e validados, sugere-se que a variante rs1433099 no gene LDLR seja incorporada nos exames genéticos associadas a essa patologia; possibilitando a expansão do diagnóstico, além do tratamento precoce dessa enfermidade tão frequente.

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