Purple passion fruit (Passiflora edulis f. edulis): a comprehensive review on the nutritional value, phytochemical profile and associated health effects

Passiflora is a highly diverse genus where taxonomic lack of consensus remains. This may be the reason why numerous studies do not specify to the infraspecific level the plant material used or lack consistency in the nomenclature of botanical formae of Passiflora edulis. Ultimately, this may contribute to inaccurate chemical composition and health effects attributed to different Passiflora edulis species and formae. Hence, this review aims to overcome these challenges by exploring the phytochemical profile, specific nutritional value and potential health benefits of purple passion fruit (PPF). PPF is often consumed fresh for its pulp (including seeds) or juice, either directly or added to food dishes. It is also used industrially to produce a wide range of products, where peels and seeds are abundant by-products, most often discarded or used in low-value applications. Herein, in a perspective of integral valorisation of the fruit, the potential use of all PPF fractions (peel, pulp and seeds) is discussed as a source of important macro and micronutrients, adequate to integrate a balanced and healthy diet. In addition, the phytochemical profile of such fractions is also discussed along with the associated in vitro biological activities (antioxidant, anti-inflammatory, antibacterial and antifungal) and in vivo beneficial effects in the management of several diseases (asthma, hypertension, osteoarthritis, diabetes and pulmonary fibrosis). In summary, this review gathers the current knowledge on the nutritional and phytochemical composition of PPF and highlights the potential of using all fractions as a source of ingredients in food formulations that promote health and well-being. At the same time, it also contributes to defining sustainable strategies for an integrated valorisation of this natural product.publishe

Efeito da pré-embebição das sementes e do substrato na germinação e no desenvolvimento inicial do maracujazeiro-doce.

O objetivo deste trabalho foi avaliar o efeito da pré-embebição das sementes em água e do tipo de substrato na germinação e no desenvolvimento inicial do maracujazeiro-doce (P. alata Curtis). O trabalho foi realizado no Departamento de Fitotecnia, da Universidade Federal de Viçosa (MG). As sementes foram extraídas de frutos maduros, e somente uma porção foi embebida em água destilada, durante 24 horas. Posteriormente, no interior da casa de vegetação, as sementes foram semeadas em caixas plásticas, utilizando-se quatro substratos (areia; Plantmax?; torta de filtro e a mistura Plantmax + areia + torta de filtro (1:1:1 v/v). Foi utilizado o delineamento experimental em blocos casualizados, num fatorial 2 x 4 (pré-embebição x substrato), com quatro repetições, considerando como unidade experimental cada 50 sementes. Aos 33 dias após a semeadura, foram analisados: porcentagem de germinação e de sobrevivência das plântulas; número de folhas; comprimento total e comprimento de raiz das plântulas; índice de velocidade de emergência; e massa da matéria seca total das plântulas. Concluiu-se que a embebição das sementes em água não interferiu na germinação do maracujazeiro-doce. Em geral, obtiveram-se os maiores resultados nas variáveis analisadas quando se utilizou o substrato comercial Plantmax, sendo seu uso recomendado para formação de plântulas de maracujazeiro-doce

IMPORTÂNCIA DA REGIÃO ANTEROVENTRAL DO TERCEIRO VENTRÍCULO (AV3V) NO CONTROLE CARDIOVASCULAR E DO EQUILÍBRIO HIDROELETROLÍTICO

A manutenção da pressão arterial em níveis normais é importante para a homeostasia do meio interno. O sistema nervoso central regulando a atividade dos eferentes autonômicos simpático e parassimpático ajusta a pressão arterial possibilitando ao animal ou ao ser humano um melhor desempenho frente a diferentes situações do cotidiano. Diferentes áreas centrais são responsáveis pelo controle das descargas autonômicas sobre o sistema cardiovascular e muitas delas também participam do controle do equilíbrio hidroeletrolítico. Uma dessas áreas é o tecido periventricular ao redor da porção anteroventral do terceiro ventrículo (região AV3V) localizado no prosencéfalo e que é uma das principais áreas centrais onde se localizam receptores da angiotensina II e osmorreceptores. A lesão da região AV3V impede o desenvolvimento de diversas formas de hipertensão experimental em ratos e dificulta o aparecimento de respostas pressoras produzidas por diversos estímulos. A lesão da região AV3V também reduz respostas dipsogênicas induzidas pela angiotensina II, estimulação colinérgica central, privação hídrica e aumento de osmolaridade plasmática, a secreção do peptídeo natriurético atrial produzida pela expansão de volume e a excreção renal de sódio produzida pela estimulação colinérgica central. Evidências mais recentes também sugerem uma participação da região AV3V nas respostas pressoras produzidas pela ativação de mecanismos bulbares.The maintenance of the arterial pressure in normal levels is important for the homeostasis of body fluids. The central nervous system regulating sympathetic and parasympathetic autonomic efferent can adjust arterial pressure which allows animals or human to face different daily activities with the best performance. Different central areas are responsible for the control of autonomic discharges to cardiovascular system and many of them are also involved in the control of fluid electrolyte balance. One of these areas is the tissue surrounding the anteroventral third ventricle (AV3V region) localized in the forebrain and a main central site for angiotensin II receptors and osmoreceptors. The AV3V lesions impair the development of many models of experimental hypertension in rats and the pressor responses to different stimuli. Lesions of the AV3V region also reduce dipsogenic responses to angiotensin II, central cholinergic activation, water deprivation and increase in plasma osmolarity, atrial natriuretic peptide secretion produced by body fluid expansion and the increase in renal excretion to central cholinergic activation. Recent evidence also suggests the participation of AV3V region in pressor responses produced by the  activation of medullary mechanisms

Analysis of unbound plasma concentration of oxcarbazepine and the 10-hydroxycarbazepine enantiomers by liquid chromatography with tandem mass spectrometry in healthy volunteers

This study describes the development and validation of a method for the analysis of unbound plasma concentrations of oxcarbazepine (OXC) and of the enantiomers of its active metabolite 10-hydroxycarbazepine (MHD) [S-(+)- and R-(−)-MHD] using liquid chromatography with tandem mass spectrometry (LC–MS/MS). Additionally, the free fraction of the drug is described in healthy volunteers (n = 12) after the oral administration of 300 mg OXC/12 h for 5 days. Plasma aliquots of 200 μL were submitted to ultrafiltration procedure and 50 μL of the ultrafiltrate were extracted with a mixture of tert-butyl methyl ether:dichloromethane (2:1, v/v). OXC and the MHD enantiomers were separated on a OD-H chiral phase column. The method was linear in the range of 4.0–2.0 μg/mL for OXC and of 20.0–6.0 μg/mL plasma for the MHD enantiomers. The limit of quantification was 4 ng for OXC and 20 ng for each MHD enantiomer/mL plasma. The intra- and inter-day precision and inaccuracy were less than 15%. The free fraction at the time of peak plasma concentration of OXC was 0.27 for OXC, 0.37 for S-(+)-MHD and 0.42 for R-(−)-MHD. Enantioselectivity in the free fraction of MHD was observed, with a higher proportion of R-(−)-MHD compared to S-(+)-MHD

Effects of previous carbohydrate supplementation on muscular fatigue: double-blind, randomized, placebo-controlled crossover study

Abstract AIMS The aim of this study was to examine the effects of previous carbohydrate supplementation on high-volume resistance exercise performance METHODS Twenty males physically independent adults aged ≥18 years participated in a double-blind randomized placebo-controlled crossover study. Sixty minutes before the experimental protocol, each participant ingested 0,6 g.kg of body mass-1 of carbohydrate supplementation or placebo. Maximum voluntary isometric contraction tests were performed before and after the dynamic fatigue induction protocol consisting of 10 sets of 8 repetitions of right leg knee extensors at 120º s-1. RESULTS Lower decrement of the isometric peak torque (p<0,001) and of the rate of torque development (p<0,001) was observed in carbohydrate supplementation after the dynamic protocol. Both concentric and eccentric peak torque differed significantly (p<0,001) between carbohydrate supplementation and placebo treatments from the second set, although the slope of the force-repetitions curve was not different between them. Additionally, the carbohydrate supplementation resulted in a lower session rating of perceived exertion (p<0,05). CONCLUSIONS Previous carbohydrate supplementation attenuates muscle fatigue and internal load exercise in a high-volume isokinetic leg protocol

Description of training loads using whole body exercise during high-intensity-interval-training

OBJECTIVES: To describe external training load and internal training load through sets of a single session of high-intensity interval training (HIIT) body work. METHODS: Twenty male individuals (24±3 years) performed a HIIT body work protocol consisting of a single bout of exercise with 1:1 stimuli. The exercises used were 30 min in duration with “all-out” intensity. The exercises included jumping jacks, mountain climbers, burpees and squat jumps, totaling 20 min of exercise. During exercise, total movement capacity, blood lactate measurement, ratings of perceived exertion and recovery, training load and intensity were monitored. RESULTS: The single bout examined showed a total of 382±89 movements. Differences (p<0.01) in the total amount of movement for each exercise were noted, reflecting the difficulty of maintaining exercise over time. Increases in lactate concentrations (before: 0.98±0.16, after: 14.10±1.66; mmol/L) were found postexercise. Significant differences (p<0.01) were found after the fifth set, and the values for movement capacity remained higher than the values of the first set, demonstrating high load in a single session. No differences in ratings of perceived exertion (RPE) during the sets were found. However, the ratings of perceived recuperation from the second set were significantly (p<0.01) lower than those from the first set. CONCLUSIONS: The exercise protocol used in this study was of high intensity and produced large values for stress during performance, with increases recorded for the internal load indicators

Post-mortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographic, etiologic and histological pulmonary analysis

Introduction: Acute respiratory failure (ARF) is present in 5% of the patients with acute myocardial infarction (AMI) and is responsible for 20% to 30% of the mortality post-AMI. It is unclear the role of inflammation correlated with pulmonary edema (PE) as a cause of ARF post-AMI. Objectives: Describe the demographic, etiologic data and histological pulmonary findings in autopsies of patients dead due to ARF with non-diagnosis AMI during life between 1,990 and 2,008. Methods: This study considers 4,223 autopsies of patients who died of ARF without cause of death related during life. The diagnosis of AMI was performed in 218 (4.63%) patients, and were obtained: age, sex and major associated diseases. Pulmonary histopathology was categorized as: diffuse alveolar damage (DAD); pulmonary edema (PE); alveolar hemorrhage (AH);and lympho-plamacytic interstitial pneumonia (LPIP). Odds ratio of AMI developing specific histopathology was determined by logistic regression. Results: Were observed 147 men and mean age was 64 years. Pulmonary histopathology showed, in descending order: PE (72.9%), DAD, LPIP and HA. Bacterial bronchopneumonia was present in 11.9%, systemic arterial hypertension in 10.1%, dilated cardiomyopathy in 6.9%, pulmonary embolism in 6.0%, hypertrophic cardiomyopathy in 4.6%, chronic obstructive pulmonary disease in 3.7% and diabetes mellitus in 3.7% of patients. Multivariate analysis demonstrated significantly positive association of IAM with PE and with DAD. Conclusions: For the first time we demonstrated that in autopsies of patients with ARF as cause of death, the diagnosis of AMI was present in about 5%. We observed important inflammatory response in pulmonary histology as never suggested beforeIntrodução: A insuficiência respiratória aguda (IRA) está presente em 5% dos pacientes com infarto agudo do miocárdio (IAM) e é associada à mortalidade de 20% a 30% nesses pacientes. Não está claro o papel da inflamação relacionada ao edema agudo de pulmão (EAP) na gênese da IRA pós IAM. Objetivos: Descrever os dados demográficos, etiológicos e os achados histológicos pulmonares em autópsias realizadas uentre 1990 e 2008, de pacientes que morreram por IRA, sem diagnóstico in-vivo de IAM. Métodos: Este estudo considerou 4223 autópsias de pacientes que morreram de IRA nos quais só foi definida post-mortem sua causa de morte. O diagnóstico de IAM foi feito por autópsia em 218 (4,63%) pacientes, dos quais foram obtidos: idade, sexo e principais doenças associadas. Os achados pulmonares histológicos foram classificados em: dano alveolar difuso (DAD), edema agudo de pulmão (EAP), hemorragia alveolar (HA) e pneumonia intersticial linfo-plasmocitária (PILP). A probabilidade de IAM desenvolver determinado tipo de achado histopatológico pulmonar foi calculada por regressão logística. Resultados: Foram observados 147 homens, e a mediana de idade foi 64 anos. A análise histopatológica pulmonar mostrou, em ordem decrescente: EAP (72,9%), DAD, PILP e HIA. Broncopneumonia bacteriana esteve presente em 11,9%, hipertensão arterial sistêmica em 10,1%, miocardiopatia dilatada em 6,9%, tromboembolismo pulmonar em 6,0%, cardiomiopatia hipertrófica em 4,6%, doença pulmonar obstrutiva crônica em 3,7% e diabetes mellitus em 3,7% dos pacientes. A análise multivariada demonstrou associação significativamente positiva de IAM com EAP e DAD. Conclusões: Pela primeira vez na literatura, demonstramos, por meio de autópsias, que em pacientes com IRA que evoluem à óbito sem diagnóstico estabelecido, IAM esteve presente em aproximadamente 5% dos casos. Nós observamos importante componente inflamatório na histologia pulmonar, nunca antes sugerid

Population pharmacokinetics of oxcarbazepine and its metabolite 10-hydroxycarbazepine in healthy subjects

Oxcarbazepine is indicated for the treatment of partial or generalised tonic-clonic seizures. Most of the absorbed oxcarbazepine is converted into its active metabolite, 10-hydroxycarbazepine (MHD), which can exist as R-(-)- and S-(+)-MHD enantiomers. Here we describe the influence of the P-glycoprotein (P-gp) inhibitor verapamil, on the disposition of oxcarbazepine and MHD enantiomers, both of which are P-gp substrates. Healthy subjects (n=12) were randomised to oxcarbazepine or oxcarbazepine combined with verapamil at doses of 300mg b.i.d. and 80mg t.i.d., respectively. Blood samples (n=185) were collected over a period of 12h post oxcarbazepine dose. An integrated PK model was developed using nonlinear mixed effects modelling using a meta-analytical approach. The pharmacokinetics of oxcarbazepine was described by a two-compartment model with absorption transit compartments and first-order elimination. The concentration-time profiles of both MHD enantiomers were characterised by a one-compartment distribution model. Clearance estimates (95% CI) were 84.9L/h (69.5-100.3) for oxcarbazepine and 2.0L/h (1.9-2.1) for both MHD enantiomers. The volume of distribution was much larger for oxcarbazepine (131L (97-165)) as compared to R-(-)- and S-(+)-MHD (23.6L (14.4-32.8) vs. 31.7L (22.5-40.9), respectively). Co-administration of verapamil resulted in a modest increase of the apparent bioavailability of oxcarbazepine by 12% (10-28), but did not affect parent or metabolite clearances. Despite the evidence of comparable systemic levels of OXC and MHD following administration of verapamil, differences in brain exposure to both moieties cannot be excluded after P-glycoprotein inhibition

In the matter of the request of Liberty Mutual Fire Insurance Company, a Massachusetts domestic stock insurance company, to redomesticate to the state of Wisconsin

Submitted by Nuzia Santos ([email protected]) on 2018-08-24T16:36:28Z No. of bitstreams: 1 Phosphatidyl Inositol 3 Kinase-Gamma Balances.pdf: 10035595 bytes, checksum: 5a61fb2c618990d4314d36db3868ee2e (MD5)Approved for entry into archive by Nuzia Santos ([email protected]) on 2018-08-24T16:44:27Z (GMT) No. of bitstreams: 1 Phosphatidyl Inositol 3 Kinase-Gamma Balances.pdf: 10035595 bytes, checksum: 5a61fb2c618990d4314d36db3868ee2e (MD5)Made available in DSpace on 2018-08-24T16:44:27Z (GMT). No. of bitstreams: 1 Phosphatidyl Inositol 3 Kinase-Gamma Balances.pdf: 10035595 bytes, checksum: 5a61fb2c618990d4314d36db3868ee2e (MD5) Previous issue date: 2018Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Vírus Respiratórios e do Sarampo. Rio de Janeiro, RJ, Brazil / Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil / Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Fisiologia e Biofísica. Laboratório de Imunologia e Mecânica Pulmonar. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brazil / UNIFRANZ. Coordinación Nacional de Investigación. La Paz, Bolivia.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Morfologia. Belo Horizonte, MG, BrazilUniversidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil / Universidade de São Paulo. Departamento de Farmacologia. Laboratório de Inflamação e Dor. Universidade de São Paulo. Ribeirão Preto, SP, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Vírus Respiratórios e do Sarampo. Rio de Janeiro, RJ, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil / Fundação Oswaldo Cruz. Instituto René Rachou. Laboratório de Imunologia de Doenças Virais. Belo Horizonte, MG, BrazilUniversidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil / Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Biologia Geral. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de RNA de Interferência Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Vírus Respiratórios e do Sarampo. Rio de Janeiro, RJ, Brazil.Fundação Oswaldo Cruz. Instituto René Rachou. Laboratório de Imunologia de Doenças Virais. Belo Horizonte, MG, BrazilUniversidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil / Universidade Federal de Minas Gerais. Faculdade de Farmácia. Departamento de Análises Clínicas e Toxicológicas. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil / Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Fisiologia e Biofísica. Laboratório de Imunologia e Mecânica Pulmonar. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, Brazil.Influenza A virus (IAV) infection causes severe pulmonary disease characterized by intense leukocyte infiltration. Phosphoinositide-3 kinases (PI3Ks) are central signaling enzymes, involved in cell growth, survival, and migration. Class IB PI3K or phosphatidyl inositol 3 kinase-gamma (PI3Kγ), mainly expressed by leukocytes, is involved in cell migration during inflammation. Here, we investigated the contribution of PI3Kγ for the inflammatory and antiviral responses to IAV. PI3Kγ knockout (KO) mice were highly susceptible to lethality following infection with influenza A/WSN/33 H1N1. In the early time points of infection, infiltration of neutrophils was higher than WT mice whereas type-I and type-III IFN expression and p38 activation were reduced in PI3Kγ KO mice resulting in higher viral loads when compared with WT mice. Blockade of p38 in WT macrophages infected with IAV reduced levels of interferon-stimulated gene 15 protein to those induced in PI3Kγ KO macrophages, suggesting that p38 is downstream of antiviral responses mediated by PI3Kγ. PI3Kγ KO-derived fibroblasts or macrophages showed reduced type-I IFN transcription and altered pro-inflammatory cytokines suggesting a cell autonomous imbalance between inflammatory and antiviral responses. Seven days after IAV infection, there were reduced infiltration of natural killer cells and CD8+ T lymphocytes, increased concentration of inflammatory cytokines in bronchoalveolar fluid, reduced numbers of resolving macrophages, and IL-10 levels in PI3Kγ KO. This imbalanced environment in PI3Kγ KO-infected mice culminated in enhanced lung neutrophil infiltration, reactive oxygen species release, and lung damage that together with the increased viral loads, contributed to higher mortality in PI3Kγ KO mice compared with WT mice. In humans, we tested the genetic association of disease severity in influenza A/H1N1pdm09-infected patients with three potentially functional PIK3CG single-nucleotide polymorphisms (SNPs), rs1129293, rs17847825, and rs2230460. We observed that SNPs rs17847825 and rs2230460 (A and T alleles, respectively) were significantly associated with protection from severe disease using the recessive model in patients infected with influenza A(H1N1)pdm09. Altogether, our results suggest that PI3Kγ is crucial in balancing antiviral and inflammatory responses to IAV infection