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Id: biblio-1283634
Autor: Dutta, Subhajit; Delpiano, Marco A.
Título: Neuroprotective natural products: promising candidates against neurodegenerative diseases / Productos naturales con propiedades neuroprotectivas: posibles candidatos para el tratamiento de enfermedades neurodegenerativas
Fonte: Bol. latinoam. Caribe plantas med. aromát;19(5):466-481, 2020. ilus, tab.
Idioma: en.
Resumo: Neurodegeneration is a progressive loss of neurons both structurally and functionally causing neuronal cell death ultimately leading to development of various neurodegenerative diseases. Due to poor pharmacokinetic profile of neurotrophins, there still remains a challenge in their neurotrophic therapy where plants, bacteria and fungi, as natural products, could act as promising candidates against various neurological disorders by modulating the neurotrophic activity. Therefore, these natural products that mimic neurotrophins, could develop novel therapeutic approaches to herbal drug that can ameliorate neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease and other associated neurological disorders. Taking into account the failure of strategies involving single neurotrophins for the treatment of neurodegenerative diseases, we propose a combination of small molecules of natural products that may work synergistically to restore neuronal functions, minimize side effects and target multiple pathways for a more effective treatment.

La neurodegeneración es una pérdida progresiva de neuronas, tanto estructural como funcional, que causa la muerte neuronal, lo que conduce al desarrollo de diversas enfermedades neurodegenerativas. Debido al pobre perfil farmacocinético de las neurotrofinas, existe un desafío en su terapia neurotrófica donde plantas, bacterias y hongos, como productos naturales, podrían actuar como candidatos contra diversos trastornos neurológicos al modular la actividad neurotrófica. Estos productos naturales que asemejan a las neurotrofinas podrían desarrollar enfoques terapéuticos novedosos como medicamentos a base de hierbas que pueden mejorar enfermedades neurodegenerativas como: Parkinson, Alzheimer y otros trastornos neurológicos asociados. Teniendo en cuenta el fracaso de las estrategias terapéuticas de neurotrofinas para las enfermedades neurodegenerativas, proponemos una combinación de pequeñas moléculas de productos naturales que pueden funcionar sinérgicamente para restaurar las funciones neuronales, minimizar los efectos secundarios y apuntar a múltiples vías para un tratamiento más efectivo.
Descritores: Produtos Biológicos/uso terapêutico
Fármacos Neuroprotetores/uso terapêutico
Doenças Neurodegenerativas/tratamento farmacológico
-Doença de Parkinson/tratamento farmacológico
Transdução de Sinais
Doença de Alzheimer/tratamento farmacológico
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1047333
Autor: Medeiros, Alessandra; Montrezol, Fábio Tanil.
Título: Efeito do treinamento físico no coração / Effect of exercise training on heart
Fonte: Rev. Soc. Cardiol. Estado de Säo Paulo;29(4,Supl):400-407, out.-dez. 2019.
Idioma: pt.
Resumo: O coração é um órgão que se adapta frente aos diferentes estímulos ou desafios a que é exposto. No entanto, o tipo de adaptação e a magnitude da mesma dependem do tipo, da magnitude e do tempo de duração do estímulo. Logo, a adaptação cardíaca observada após um período de treinamento físico é diferente da adaptação cardíaca observada nas doenças cardiovasculares. Além disso, as variáveis inerentes ao exercício físico como tipo, intensidade, volume e frequência semanal também apresentam uma relação direta quanto ao tipo de adaptação cardíaca. No presente artigo revisaremos os efeitos dos diferentes tipos treinamento físico na estrutura e função cardíaca, abordando os diferentes tipos de hipertrofia cardíaca (excêntrica e concêntrica), bem como as principais vias de sinalização intracelular responsáveis por essa hipertrofia. Além disso, abordaremos como alguns dos principais fatores (massa corporal, sexo, etnia e fatores genéticos) influenciam na magnitude da hipertrofia cardíaca e discutiremos se o treinamento físico praticado em grandes volumes pode ser prejudicial à saúde cardíaca

The heart is an organ that adapts to the different stimuli or challenges to which it is exposed. However, the type of adaptation and its magnitude depend on the stimulus type, magnitude and duration. Therefore, the cardiac adaptation observed after a period of exercise training is different from the cardiac adaptation observed in cardiovascular diseases. In addition, the variables inherent in exercise training such as type, intensity, volume and weekly frequency also have a direct relation to the type of cardiac adaptation. In this article we will review the effects of different types of exercise training on cardiac structure and function, addressing the different types of cardiac hypertrophy (eccentric and concentric), as well as the main intracellular signaling pathways responsible for this hypertrophy. In addition, we will discuss how some of the major factors (body mass, gender, ethnicity, and genetic factors) influence the magnitude of cardiac hypertrophy and will discuss whether high-volume of exercise training can be detrimental to heart health
Descritores: Exercício Físico
Coração
-Doenças Cardiovasculares
Sistema Cardiovascular
Transdução de Sinais
Fatores Sexuais
Fatores de Risco
Fatores Etários
MicroRNAs
Hipertensão
Hipertrofia
Tipo de Publ: Revisão
Responsável: BR44.1 - Serviço de Biblioteca, Documentação Científica e Didática Prof. Dr. Luiz Venere Décourt


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Id: biblio-1152068
Autor: Pimentel, Adriana.
Título: Efecto de esfingolípidos y Agelosina B en la movilización de Ca2+ y la señalización celular en células de cáncer de mama (MCF-7) y su relación con la apoptosis / Effect of sphingolipids and Agelosin B on Ca2 + mobilization and cell signaling in breast cancer cells (MCF-7) and its relationship with apoptosis.
Fonte: Caracas; s.n; oct. 2011. 185 p. ilus. (LFT-4872011615789).
Idioma: es.
Tese: Apresentada a Universidad Central de Venezuela. Facultad de Farmacia para obtenção do grau de Doctor.
Símbolo: LFT-4872011615789.
Resumo: Los esfingolípidos, como la ceramida (Cer), la ceramida-1-fosfato (C-1-P), la esfingosina (Sph) y la esfingosina-1-fosfato (S-1P) estan relacionados con la señalización intracelular en procesos como crecimiento celular, movilización intracelular de Ca+2 y apoptósis. En este trabajo se evaluó el efecto de estos esfingolípidos en la homeostasis de Ca+2 intracelular y en la apoptósis en células de cáncer de mama MCF-7. Se utilizaron fluoróforos específicos para el Ca+2 y microscopía confocal. Se demostró que en estas células, la Sph (20 uM), la Cer (10uM), la S-P (2uM) y la C--P (uM) aumentaron la concentración intracelular ce Ca+2, induciendo su liberación desde el retículo endoplasmático (RE). Además, se observo que la esfingosina abrioun canal de Ca2+ en la membrana plasmática. También se demostró que la Cer inhibe parcialmente la actividad de la Ca2+-ATPasa del RE (SERCA), de forma dosis dependiente, mientras que la ceramina, su análogo no hidrolisable la inhibe totalmente. La Sph también inhibe completamente la actividad de la SERCA, a la misma concentración que induce la liberación del Ca+2 del RE. Asimismo, se evaluó el efecto de estos esfingolípidos sobre la inducción de la apotósis en células MCF-7 evidenciando que el tratamiento con la Cer, la ceramida, la Sph inducen toxicidad. También se observo que mientras la ceramida activo la caspasa 7 y la caspasa 8, el esfingolipido natural, la Cer no tuvo ningún efecto. Por su parte, la Sph activa la caspasa 8 sin modificar la activdad de la caspasa 7. Tanto la Cer, como la ceramida y la Sph, disminuyeron la expresión de la proteína Bcl-2 amti-apoptótica, y también indujeron la fragmentación de ADN, visualizada mediante la técnica de TUNEL, demostrando que estos esfingolípidos inducen apoptósis en MCF-7. La agelasina B, toxina purificada a partir de la esponja marina Agelas clathrodes tiene un efecto citotóxico un orden de magnitud mayor en MCF-7, en comparación con fibroplastos humanos. La agelasina B induce la liberación del Ca+2 almacenado en el RE en celulas MCF-7, ademas de inhibir la actividad de la SERCA en un 100%. También se demostró que esta toxina induce apoptosis, ya que disminuye el potencial de membrana mitocondrial, activa la caspasa 8, disminuye la expresion de la proteina Bcl-2 e induce fragmentación del ADN de las células MCF-7. Este mecanismo es similar al efecto de la tapsigargina.
Descritores: Esfingolipídeos/farmacologia
Neoplasias da Mama/metabolismo
Transdução de Sinais/efeitos dos fármacos
Cálcio/metabolismo
Apoptose/efeitos dos fármacos
Agelas/química
-Purinas/uso terapêutico
Purinas/farmacologia
Esfingolipídeos/toxicidade
Esfingolipídeos/uso terapêutico
Neoplasias da Mama/patologia
Neoplasias da Mama/tratamento farmacológico
Ceramidas/toxicidade
ATPases Transportadoras de Cálcio/efeitos adversos
Marcação In Situ das Extremidades Cortadas/métodos
Receptores de Detecção de Cálcio/uso terapêutico
Células MCF-7
Naftalenos/uso terapêutico
Naftalenos/farmacologia
Antineoplásicos/uso terapêutico
Antineoplásicos/farmacologia
Limites: Humanos
Animais
Tipo de Publ: Ensaio Clínico Controlado
Responsável: VE497.1 - Biblioteca Dr. Oswaldo Enríquez Isava
VE497.1; D-CF, P5


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Id: biblio-1045825
Autor: Cai, H; Chen, Q; Liu, Y; Xie, H; Lu, Q; Chen, X.
Título: The Application Methods of Mitogen-activated Protein Kinase Signal Pathway Inhibitors SP600125 and SB203580 in Long-term in Vivo Experiments / Métodos de aplicación de los inhibidores SP600125 y SB203580 de la vía de señalización de la proteína quinasa activada por mitógeno en experimentos in vivo a largo plazo
Fonte: West Indian med. j;67(2):98-104, Apr.-June 2018. tab, graf.
Idioma: en.
Projeto: Chinese Natural Science Foundation; . Scientific Fund of Hunan Provincial Education Department.
Resumo: ABSTRACT Objective: To explore the application methods of mitogen-activated protein kinase signal pathway inhibitors SP600125 and SB203580 in long-term in vivo experiments. Methods: A total of 55 healthy New Zealand rabbits were randomly divided into blank control group, model control group, SP low dose group, SP high dose group, SP blank group, SB low dose group, SB high dose group, SB blank group, dimethyl sulfoxide (DMSO) control group, DMSO blank group, and positive control group. Since the first day of the experiment, each group was administered the corresponding treatment for four weeks continuously. Then, the myocardial c-Jun N-terminal kinase (JNK) and the total protein of p38, protein phosphorylation and its gene expression levels were detected. Results: After intravenous treatment with adriamycin, the myocardial phosphorylate-JNK (p-JNK) and phosphorylate-p38 (p-p38) levels in all groups were increased to varying degrees, of which the model control group increased the most significantly (p < 0.05). Compared with the model control group, the myocardial p-JNK and p-p38 increased more slowly in the SP low dose group, SP high dose group, SB low dose group, SB high dose group and positive control group (p < 0.05), of which the increase in the SP high dose group and the SB high dose group was the slowest (p < 0.05). After four weeks, the total protein and messenger ribonucleic acid of the myocardial JNK and p38 in all groups had no statistically significant difference (p > 0.05). Conclusion: The continuous intravenous injection of SP600125 and SB203580 for four weeks significantly reduced the protein phosphorylation levels of JNK and p38, which provides a practical avenue for the long-term study in vivo.

RESUMEN Objetivo: Explorar los métodos de aplicación de los inhibidores SP600125 y SB203580 de la vía de señalización de la proteína quinasa activada por mitógeno en experimentos in vivo a largo plazo. Métodos: Un total de 55 conejos sanos de Nueva Zelandia fueron divididos aleatoriamente en los grupos siguientes: grupo de control en blanco, grupo de control modelo, grupo de dosis baja SP, grupo de dosis alta SP, grupo en blanco SP, grupo de dosis baja SB, grupo de dosis alta SB, grupo en blanco SB, grupo de control dimetilsulfóxido (DMSO), grupo en blanco DMSO, y grupo de control positivo. Desde el primer día del experimento, a cada grupo se le administró el tratamiento correspondiente por cuatro semanas continuas. Entonces, se detectaron la quinasa c-Jun N-terminal (JNK) miocárdica y la proteína p38 total, así como la fosforilación proteica y sus niveles de expresión génica. Resultados: Después del tratamiento intravenoso con adriamicina, los niveles de fosfo-JNK (p-JNK) y fosfo-p38 (p-p38) del miocardio aumentaron en todos los grupos en diversos grados, siendo el aumento del grupo de control modelo el más significativo (p < 0.05). En comparación con el grupo de control modelo, p-JNK y p-p38 miocárdicos aumentaron más lentamente en el grupo de dosis baja SP, el grupo de dosis alta SP, el grupo de dosis baja SB, el grupo de dosis alta SB, y el grupo de control positivo (p < 0.05). De estos, el aumento en el grupo de dosis alta SP y el grupo de dosis alta SB fue el más lento (p < 0.05). Después de cuatro semanas, la proteína total y el ácido ribonucleico mensajero de JNK y p38 miocárdicos en todos los grupos, no tuvieron diferencias significativas (p > 0.05). Conclusión: La inyección intravenosa continua de SP600125 y SB203580 durante cuatro semanas redujo significativamente los niveles de fosforilación proteica de JNK y p38, lo que proporciona una vía práctica para el estudio a largo plazo in vivo.
Descritores: Doxorrubicina/farmacologia
Proteínas Quinases Ativadas por Mitógeno/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
-Fosforilação/efeitos dos fármacos
Fatores de Tempo
Transdução de Sinais/efeitos dos fármacos
Distribuição Aleatória
Expressão Gênica
Limites: Humanos
Masculino
Coelhos
Responsável: BR1.1 - BIREME


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Id: biblio-952823
Autor: Russo, Lilian Cristina; Farias, Jéssica Oliveira; Ferruzo, Pault Yeison Minaya; Monteiro, Lucas Falcão; Forti, Fábio Luís.
Título: Revisiting the roles of VHR/DUSP3 phosphatase in human diseases
Fonte: Clinics;73(supl.1):e466s, 2018. graf.
Idioma: en.
Projeto: Grant.
Resumo: Protein tyrosine phosphatases have long been considered key regulators of biological processes and are therefore implicated in the origins of various human diseases. Heterozygosity, mutations, deletions, and the complete loss of some of these enzymes have been reported to cause neurodegenerative diseases, autoimmune syndromes, genetic disorders, metabolic diseases, cancers, and many other physiological imbalances. Vaccinia H1-related phosphatase, also known as dual-specificity phosphatase 3, is a protein tyrosine phosphatase enzyme that regulates the phosphorylation of the mitogen-activated protein kinase signaling pathway, a central mediator of a diversity of biological responses. It has been suggested that vaccinia H1-related phosphatase can act as a tumor suppressor or tumor-promoting phosphatase in different cancers. Furthermore, emerging evidence suggests that this enzyme has many other biological functions, such as roles in immune responses, thrombosis, hemostasis, angiogenesis, and genomic stability, and this broad spectrum of vaccinia H1-related phosphatase activity is likely the result of its diversity of substrates. Hence, fully identifying and characterizing these substrate-phosphatase interactions will facilitate the identification of pharmacological inhibitors of vaccinia H1-related phosphatase that can be evaluated in clinical trials. In this review, we describe the biological processes mediated by vaccinia H1-related phosphatase, especially those related to genomic stability. We also focus on validated substrates and signaling circuitry with clinical relevance in human diseases, particularly oncogenesis.
Descritores: Fosfatase 3 de Especificidade Dupla/fisiologia
Neoplasias/enzimologia
-Transdução de Sinais
Análise de Sobrevida
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Neoplasias/mortalidade
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: biblio-974958
Autor: Machado-Neto, João Agostinho; Fenerich, Bruna Alves; Rodrigues Alves, Ana Paula Nunes; Fernandes, Jaqueline Cristina; Scopim-Ribeiro, Renata; Coelho-Silva, Juan Luiz; Traina, Fabiola.
Título: Insulin Substrate Receptor (IRS) proteins in normal and malignant hematopoiesis
Fonte: Clinics;73(supl.1):e566s, 2018. tab, graf.
Idioma: en.
Resumo: The insulin receptor substrate (IRS) proteins are a family of cytoplasmic proteins that integrate and coordinate the transmission of signals from the extracellular to the intracellular environment via transmembrane receptors, thus regulating cell growth, metabolism, survival and proliferation. The PI3K/AKT/mTOR and MAPK signaling pathways are the best-characterized downstream signaling pathways activated by IRS signaling (canonical pathways). However, novel signaling axes involving IRS proteins (noncanonical pathways) have recently been identified in solid tumor and hematologic neoplasm models. Insulin receptor substrate-1 (IRS1) and insulin receptor substrate-2 (IRS2) are the best-characterized IRS proteins in hematologic-related processes. IRS2 binds to important cellular receptors involved in normal hematopoiesis (EPOR, MPL and IGF1R). Moreover, the identification of IRS1/ABL1 and IRS2/JAK2V617F interactions and their functional consequences has opened a new frontier for investigating the roles of the IRS protein family in malignant hematopoiesis. Insulin receptor substrate-4 (IRS4) is absent in normal hematopoietic tissues but may be expressed under abnormal conditions. Moreover, insulin receptor substrate-5 (DOK4) and insulin receptor substrate-6 (DOK5) are linked to lymphocyte regulation. An improved understanding of the signaling pathways mediated by IRS proteins in hematopoiesis-related processes, along with the increased development of agonists and antagonists of these signaling axes, may generate new therapeutic approaches for hematological diseases. The scope of this review is to recapitulate and review the evidence for the functions of IRS proteins in normal and malignant hematopoiesis.
Descritores: Transdução de Sinais/fisiologia
Leucemia Linfoide/metabolismo
Leucemia Mieloide/metabolismo
Proteínas Substratos do Receptor de Insulina/metabolismo
Hematopoese/fisiologia
-Leucemia Linfoide/fisiopatologia
Leucemia Mieloide/fisiopatologia
Proteínas Substratos do Receptor de Insulina/fisiologia
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: biblio-989635
Autor: Ghani, Siti Madiani Abdul; Goon, Jo Aan; Azman, Nor Helwa Ezzah Nor; Zakaria, Siti Nor Asyikin; Hamid, Zalina; Ngah, Wan Zurinah Wan.
Título: Comparing the effects of vitamin E tocotrienol-rich fraction supplementation and α-tocopherol supplementation on gene expression in healthy older adults
Fonte: Clinics;74:e688, 2019. tab, graf.
Idioma: en.
Projeto: UKM Economic Transformation Programme.
Resumo: OBJECTIVES This study aims to compare the differential gene expression resulting from tocotrienol-rich fraction and α-tocopherol supplementation in healthy older adults. METHODS A total of 71 eligible subjects aged 50 to 55 years from Gombak and Kuala Lumpur, Malaysia, were divided into three groups and supplemented with placebo (n=23), α-tocopherol (n=24) or tocotrienol-rich fraction (n=24). Blood samples were collected at baseline and at 3 and 6 months of supplementation for microarray analysis. RESULTS The number of genes altered by α-tocopherol was higher after 6 months (1,410) than after 3 months (273) of supplementation. α-Tocopherol altered the expression of more genes in males (952) than in females (731). Similarly, tocotrienol-rich fraction modulated the expression of more genes after 6 months (1,084) than after 3 months (596) and affected more genes in males (899) than in females (781). α-Tocopherol supplementation modulated pathways involving the response to stress and stimuli, the immune response, the response to hypoxia and bacteria, the metabolism of toxins and xenobiotics, mitosis, and synaptic transmission as well as activated the mitogen-activated protein kinase and complement pathways after 6 months. However, tocotrienol-rich fraction supplementation affected pathways such as the signal transduction, apoptosis, nuclear factor kappa B kinase, cascade extracellular signal-regulated kinase-1 and extracellular signal-regulated kinase-2, immune response, response to drug, cell adhesion, multicellular organismal development and G protein signaling pathways. CONCLUSION Supplementation with either α-tocopherol or tocotrienol-rich fraction affected the immune and drug response and the cell adhesion and signal transduction pathways but modulated other pathways differently after 6 months of supplementation, with sex-specific responses.
Descritores: Expressão Gênica/efeitos dos fármacos
Suplementos Nutricionais
alfa-Tocoferol/farmacologia
Tocotrienóis/farmacologia
Antioxidantes/farmacologia
-Proteínas Quinases/efeitos dos fármacos
Fatores de Tempo
Transdução de Sinais/efeitos dos fármacos
Adesão Celular/efeitos dos fármacos
Método Simples-Cego
Fatores Sexuais
Regulação da Expressão Gênica/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Sistema Imunitário/efeitos dos fármacos
Limites: Humanos
Masculino
Feminino
Pessoa de Meia-Idade
Tipo de Publ: Estudo Comparativo
Ensaio Clínico Controlado Aleatório
Responsável: BR1.1 - BIREME


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Id: biblio-1056491
Autor: Correa-Aravena, J; Alister, J. P; Olate, S; Manterola, C.
Título: L-PRF y Ciclo Celular. Revisión Narrativa / L-PRF and cell cycle. Narrative Review
Fonte: Int. j. odontostomatol. (Print);13(4):497-503, dic. 2019. tab, graf.
Idioma: es.
Resumo: RESUMEN: Los concentrados plaquetarios han emergido como un potencial material regenerativo, utilizado de forma aislada o como andamiaje para otros materiales de injerto. Son extractos de sangre, obtenidos después de procesar una muestra de sangre completa, mediante centrifugación. El primer reporte data de 1970, con un CP utilizado como pegamento para mejorar cicatrización de heridas de piel. En 1998, se usaron en cirugía oral y maxilofacial. Desde entonces, se han desarrollado diferentes técnicas y una variedad de preparaciones. Entre ellas, cabe destacar el plasma rico en plaquetas, fibrina rica en plaquetas y leucocitos (L-PRF) y plasma rico en factores de crecimiento (PRGF). El desarrollo de estos biomateriales, se debe en parte, a la posibilidad de alterar la concentración de mediadores químicos liberados en una lesión que provoque la formación de un coágulo, que pueda madurar conforme transcurran las fases del proceso inflamatorio y concluya con la regeneración íntegra del tejido dañado. El objetivo de este manuscrito fue describir las principales vías de señalización intracelular que se activan en presencia del L-PRF en cirugía oral, y sus efectos en la regulación del ciclo celular.

ABSTRACT: Platelet concentrates (PC) have emerged as a potential regenerative material, used in isolation or as scaffolding for other graft materials. They are blood extracts, obtained after processing a sample of whole blood, by centrifugation. The first report dates from 1970, with a PC used glue to improve the healing of skin wounds. In 1998, they were used in oral and maxillofacial surgery. Since then, different techniques and a variety of preparations have been developed. These include platelet-rich plasma, fibrin rich in platelets and leukocytes (L-PRF) and plasma rich in growth factors (PRGF). The development of these biomaterials, is due in part to the possibility of altering the concentration of chemical mediators released in a lesion that causes the formation of a clot, which can mature as the phases of the inflammatory process pass and conclude with the complete regeneration of the damaged tissue. The aim of this manuscript was to describe the main intracellular signaling pathways that are activated in the presence of LPRF in oral surgery, and its effects on the regulation of the cell cycle.
Descritores: Centrifugação
Peptídeos e Proteínas de Sinalização Intercelular
Fibrina Rica em Plaquetas
-Periodontite Periapical
Regeneração Óssea
Transdução de Sinais
Ciclinas
Fator A de Crescimento do Endotélio Vascular
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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Id: lil-613888
Autor: Mizraji, Morris; Kolenc, Francisco; Ingver, Carmela; San Millán, Julia.
Título: El sentido del gusto / The sense of taste
Fonte: Actas odontol;8(2):5-14, dic. 2011.
Idioma: es.
Resumo: El gusto es un sistema sensorial complejo que está vinculado a las conductas alimenticias del ser humano. Interactúa con el olfato, la sensibilidad táctil y térmica oral, y hasta con la visión y la audición. Se describen actualmente cinco variedades de gusto: dulce, salado, ácido, amargo y umami. Los receptores gustativos se encuentran fundamentalmente en la boca. En la transducción del estímulo gustativo participan dos mecanismos: canales iónicos para los gustos salado y ácido y receptores de membrana asociados a proteínas G para los restantes tres sabores. Se describe la vía gustativa y sus conexiones con el sistema límbicovinculadas con el placer-displacer de la gustación (hedonismo). Existen avances importantes relacionados con la codificación de los distintos estímulos gustativos, siendo la propuesta más fundamentada y aceptada la teoría de los ®patrones de actividad central¼. Algunos reflejos gustativos se producen al servicio de la masticación, por ejemplo los reflejos gustativos salivales para la formación del bolo, gustativo motor para la modulación de la frecuencia masticatoria y gustativo facial para comia y para laexpresión hedónica.

The sense of taste is a complex sensorial system related to the human feeding behavior. It interacts with the senses of smell, vision, audition and oral touch. Currently, five taste modalities are recognized: sweet, salty, sour, bitter and umami. Taste receptors are located mostly in the mouth. Two mechanisms are involved in the stimulus transduction in taste: ionic channels in the salty and sour tastes, and receptors associated to G-proteins in the transduction of the other three tastes. We describe thegustative neural pathway and their connections with the limbic system, related with the hedonic components of taste. We describe the theories advanced to explain the codification of the gustatory stimulus, with the ®central pattern activity¼ being the most accepted nowadays. Some taste reflexes have an accesory function in mastication, for example, the taste-salivary reflex helps in bolus formation, the taste-motor reflex regulates the masticatory frequency, and the gustofacial reflex helps with themastication and expresses the hedonic state.
Descritores: Canais Iônicos
Paladar/fisiologia
Transdução de Sinais/fisiologia
-Receptores Acoplados a Proteínas G
Limites: Humanos
Responsável: UY108.1 - Biblioteca Central Universidad Católica del Uruguay


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Id: biblio-950738
Autor: Kim, Sung-Jo; Hong, Minho; Song, Ki Duk; Lee, Hak-Kyo; Ryoo, Sungweon; Heo, Tae-Hwe.
Título: Normalization of the levels of inflammatory molecules in Mycobacterium smegmatis-infected U937 cells by fibrate pretreatment
Fonte: Biol. Res;47:1-9, 2014. ilus, graf.
Idioma: en.
Projeto: The Catholic University of Korea. Research Fund 2011; . Republic of Korea. Development Administration. BioGreen 21.
Resumo: BACKGROUND: Tuberculosis (TB) is a respiratory tract disease caused by Mycobacterium tuberculosis infection. M. tuberculosis exploits immune privilege to grow and divide in pleural macrophages. Fibrates are associated with the immune response and control lipid metabolism through glycolysis with ß-oxidation of fatty acids. RESULTS: In this study, we investigated the effect of fibrate pretreatment on the immune response during M. smegmatis infection in U937 cells, a human leukemic monocyte lymphoma cell line. The protein expression of tumor necrosis factor α (TNF-α), an inflammatory marker, and myeloid differentiation primary response gene 88 (MyD88), a toll like receptor adaptor molecule, in the infected group increased at 1 and 6 h after M. smegmatis infection of U937 cells. Acetyl coenzyme A acetyl transferase-1 (ACAT-1), peroxisome proliferator-activated receptor-α (PPAR-α), TNF-α, and MyD88 decreased in U937 cells treated with fibrates at 12 and 24 h after treatment. More than a 24 h pretreatment with fibrate resulted in similar expression levels of ACAT-1 and PPAR-α between infected vehicle control and infected groups which were pretreated with fibrate for 24 h. However, upon exposure to M. smegmatis, the cellular expression of the TNF-α and MyD88 in the infected groups pretreated with fibrate for 24 h decreased significantly compared to that in the infected vehicle group. CONCLUSION: These results suggest that fibrate pretreatment normalized the levels of inflammatory molecules in Mycobacterium smegmatis-infected U937 cells. Further studies are needed to confirm the findings on pathophysiology and immune defense mechanism of U937 by fibrates during M. tuberculosis infection.
Descritores: Mediadores da Inflamação/metabolismo
Mycobacterium smegmatis
Ácidos Fíbricos/farmacologia
Macrófagos/efeitos dos fármacos
Infecções por Mycobacterium/metabolismo
-Acetil-CoA C-Acetiltransferase/metabolismo
Transdução de Sinais/efeitos dos fármacos
Western Blotting
Fator de Necrose Tumoral alfa/metabolismo
Células U937
PPAR alfa/metabolismo
Fator 88 de Diferenciação Mieloide/metabolismo
Macrófagos/metabolismo
Macrófagos/microbiologia
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central



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