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1.
Nutr Hosp ; 34(5): 1267-1274, 2017 Oct 27.
Artigo em Inglês | MEDLINE | ID: mdl-29280638

RESUMO

BACKGROUND: Enteral nutrition (EN) is an effective nutritional intervention for patients at risk of malnutrition or malnourished. However, complications such as gastrointestinal intolerance, hyperglycemia or refeeding syndrome can be triggered by EN. AIM: To investigate the effects of a tube feeding formula (TFF) on patients' nutritional status, biochemical status, bowel habits and safety. METHODOLOGY: Observational, prospective and multicenter study. Patients ≥ 18 years, undernourished or at nutritional risk, who were prescribed a high-calorie, high-protein, fiber-fortified TFF were included. Patients were evaluated over a period of eight weeks (baseline [V1], four weeks [V2] and eight weeks [V3]). RESULTS: A statistically significant increase in weight (1.5 kg), body mass index (0.6 kg/m2) and nutritional intake (59.7 kcal/day) was observed between V1 and V2. Between V1 and V3, there was a statistically significant decrease in the percentage of individuals with abnormal biochemical markers for glucose, potassium, total protein and albumin. The number of patients' bowel movements remained stable throughout the study with a mean of 1.1 daily bowel movements. CONCLUSION: The TFF was safe and well tolerated, improving patients' nutritional status without altering patients' bowel habits.


Assuntos
Fibras na Dieta , Ingestão de Energia , Nutrição Enteral/métodos , Alimentos Formulados , Idoso , Idoso de 80 Anos ou mais , Defecação , Nutrição Enteral/efeitos adversos , Feminino , Alimentos Formulados/efeitos adversos , Humanos , Masculino , Estado Nutricional , Oligossacarídeos , Estudos Prospectivos , Espanha
2.
Nutr. hosp ; 34(6): 1267-1274, nov.-dic. 2017. tab, graf
Artigo em Inglês | IBECS | ID: ibc-168962

RESUMO

Background: Enteral nutrition (EN) is an effective nutritional intervention for patients at risk of malnutrition or malnourished. However, complications such as gastrointestinal intolerance, hyperglycemia or refeeding syndrome can be triggered by EN. Aim: To investigate the effects of a tube feeding formula (TFF) on patients' nutritional status, biochemical status, bowel habits and safety. Methodology: Observational, prospective and multicenter study. Patients ≥ 18 years, undernourished or at nutritional risk, who were prescribed a high-calorie, high-protein, fiber-fortified TFF were included. Patients were evaluated over a period of eight weeks (baseline [V1], four weeks [V2] and eight weeks [V3]). Results: A statistically significant increase in weight (1.5 kg), body mass index (0.6 kg/m2) and nutritional intake (59.7 kcal/day) was observed between V1 and V2. Between V1 and V3, there was a statistically significant decrease in the percentage of individuals with abnormal biochemical markers for glucose, potassium, total protein and albumin. The number of patients’ bowel movements remained stable throughout the study with a mean of 1.1 daily bowel movements. Conclusion: The TFF was safe and well tolerated, improving patients’ nutritional status without altering patients' bowel habits (AU)


Introducción: la nutrición enteral es una intervención efectiva para pacientes desnutridos o en riesgo de sufrir desnutrición. Sin embargo, puede desencadenar complicaciones como intolerancia gastrointestinal, hiperglicemia o síndrome de realimentación. Objetivo: investigar los efectos de una fórmula de nutrición enteral por sonda en el estado nutricional y bioquímico, hábitos gastrointestinales y seguridad de los pacientes. Metodología: estudio observacional, prospectivo y multicéntrico. Se incluyeron pacientes ≥ 18 años, desnutridos o en riesgo de desnutrición, tributarios de recibir una fórmula de nutrición enteral hipercalórica, hiperproteica, y rica en fibra y fructooligosacáridos. Los pacientes fueron evaluados durante 8 semanas en 3 visitas (V1, inicial; V2, 4 semanas; V3, 8 semanas). Resultados: entre V1 y V2 se observó un incremento estadísticamente significativo en peso (1,5 kg), índice de masa corporal (0,6 kg/m2) e ingesta calórica (59,7 kcal/día). Entre V1 y V3, existió un descenso en el porcentaje de pacientes con valores anormales de glucosa, potasio, proteína total y albúmina. Los hábitos intestinales se mantuvieron estables durante el estudio (1,1 deposiciones diarias de media). Conclusión: la fórmula fue segura, tolerada, y mejoró el estado nutricional del paciente sin alterar los hábitos intestinales (AU)


Assuntos
Humanos , Idoso , Idoso de 80 Anos ou mais , Estado Nutricional/fisiologia , Nutrição Enteral/métodos , Deficiência de Proteína/dietoterapia , Deficiência de Proteína/epidemiologia , Desnutrição Proteico-Calórica/dietoterapia , Oligossacarídeos/uso terapêutico , Estudos Prospectivos , 28599
3.
Oxid Med Cell Longev ; 2017: 4162465, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28706574

RESUMO

The general disruption of redox signaling following an ischemia-reperfusion episode has been proposed as a crucial component in neuronal death and consequently brain damage. Thioredoxin (Trx) family proteins control redox reactions and ensure protein regulation via specific, oxidative posttranslational modifications as part of cellular signaling processes. Trx proteins function in the manifestation, progression, and recovery following hypoxic/ischemic damage. Here, we analyzed the neuroprotective effects of postinjury, exogenous administration of Grx2 and Trx1 in a neonatal hypoxia/ischemia model. P7 Sprague-Dawley rats were subjected to right common carotid ligation or sham surgery, followed by an exposure to nitrogen. 1 h later, animals were injected i.p. with saline solution, 10 mg/kg recombinant Grx2 or Trx1, and euthanized 72 h postinjury. Results showed that Grx2 administration, and to some extent Trx1, attenuated part of the neuronal damage associated with a perinatal hypoxic/ischemic damage, such as glutamate excitotoxicity, axonal integrity, and astrogliosis. Moreover, these treatments also prevented some of the consequences of the induced neural injury, such as the delay of neurobehavioral development. To our knowledge, this is the first study demonstrating neuroprotective effects of recombinant Trx proteins on the outcome of neonatal hypoxia/ischemia, implying clinical potential as neuroprotective agents that might counteract neonatal hypoxia/ischemia injury.


Assuntos
Asfixia/complicações , Glutarredoxinas/uso terapêutico , Hipóxia-Isquemia Encefálica/metabolismo , Neurônios/patologia , Animais , Animais Recém-Nascidos , Modelos Animais de Doenças , Glutarredoxinas/administração & dosagem , Glutarredoxinas/farmacologia , Hipóxia-Isquemia Encefálica/patologia , Masculino , Ratos
4.
Biochim Biophys Acta ; 1850(6): 1274-85, 2015 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-25735211

RESUMO

BACKGROUND: Thioredoxin (Trx) family proteins are crucial mediators of cell functions via regulation of the thiol redox state of various key proteins and the levels of the intracellular second messenger hydrogen peroxide. Their expression, localization and functions are altered in various pathologies. Here, we have analyzed the impact of Trx family proteins in neuronal development and recovery, following hypoxia/ischemia and reperfusion. METHODS: We have analyzed the regulation and potential functions of Trx family proteins during hypoxia/ischemia and reoxygenation of the developing brain in both an animal and a cellular model of perinatal asphyxia. We have analyzed the distribution of 14 Trx family and related proteins in the cerebellum, striatum, and hippocampus, three areas of the rat brain that are especially susceptible to hypoxia. Using SH-SY5Y cells subjected to hypoxia and reoxygenation, we have analyzed the functions of some redoxins suggested by the animal experiment. RESULTS AND CONCLUSIONS: We have described/discovered a complex, cell-type and tissue-specific expression pattern following the hypoxia/ischemia and reoxygenation. Particularly, Grx2 and Trx1 showed distinct changes during tissue recovery following hypoxia/ischemia and reoxygenation. Silencing of these proteins in SH-SY5Y cells subjected to hypoxia-reoxygenation confirmed that these proteins are required to maintain the normal neuronal phenotype. GENERAL SIGNIFICANCE: These findings demonstrate the significance of redox signaling in cellular pathways. Grx2 and Trx1 contribute significantly to neuronal integrity and could be clinically relevant in neuronal damage following perinatal asphyxia and other neuronal disorders.


Assuntos
Asfixia Neonatal/enzimologia , Encéfalo/enzimologia , Glutarredoxinas/metabolismo , Hipóxia-Isquemia Encefálica/enzimologia , Neurônios/enzimologia , Tiorredoxinas/metabolismo , Animais , Asfixia Neonatal/patologia , Encéfalo/patologia , Linhagem Celular Tumoral , Modelos Animais de Doenças , Glutarredoxinas/genética , Humanos , Hipóxia-Isquemia Encefálica/patologia , Masculino , Neurônios/patologia , Oxirredução , Oxigênio/metabolismo , Fenótipo , Interferência de RNA , Ratos Sprague-Dawley , Transdução de Sinais , Tiorredoxinas/genética , Fatores de Tempo , Transfecção
7.
Synapse ; 67(9): 553-67, 2013 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-23447367

RESUMO

Perinatal asphyxia (PA) increases the likelihood of suffering from dopamine-related disorders, such as ADHD and schizophrenia. Since dopaminergic transmission plays a major role in cocaine sensitization, the purpose of this study was to determine whether PA could be associated with altered behavioral sensitization to cocaine. To this end, adult rats born vaginally (CTL), by caesarean section (C+), or by C+ with 15 min (PA15, moderate PA) or 19 min (PA19, severe PA) of global anoxia were repeatedly administered with cocaine (i.p., 15 mg/kg) and then challenged with cocaine (i.p., 15 mg/kg) after a 5-day withdrawal period. In addition, c-Fos, FosB/ΔFosB, DAT, and TH expression were assessed in dorsal (CPu) and ventral (NAcc) striatum. Results indicated that PA15 rats exhibited an increased locomotor sensitization to cocaine, while PA19 rats displayed an abnormal acquisition of locomotor sensitization and did not express a sensitized response to cocaine. c-Fos expression in NAcc, but not in CPu, was associated with these alterations in cocaine sensitization. FosB/ΔFosB expression was increased in all groups and regions after repeated cocaine administration, although it reached lower expression levels in PA19 rats. In CTL, C+, and PA15, but not in PA19 rats, the expression of TH in NAcc was reduced in groups repeatedly treated with cocaine, independently of the challenge test. Furthermore, this reduction was more pronounced in PA15 rats. DAT expression remained unaltered in all groups and regions studied. These results suggest that moderate PA may increase the vulnerability to drug abuse and in particular to cocaine addiction.


Assuntos
Asfixia Neonatal/complicações , Sensibilização do Sistema Nervoso Central , Transtornos Relacionados ao Uso de Cocaína/etiologia , Cocaína/farmacologia , Animais , Transtornos Relacionados ao Uso de Cocaína/metabolismo , Transtornos Relacionados ao Uso de Cocaína/fisiopatologia , Proteínas da Membrana Plasmática de Transporte de Dopamina/genética , Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo , Locomoção , Núcleo Accumbens/efeitos dos fármacos , Núcleo Accumbens/metabolismo , Proteínas Proto-Oncogênicas c-fos/genética , Proteínas Proto-Oncogênicas c-fos/metabolismo , Putamen/efeitos dos fármacos , Putamen/metabolismo , Ratos , Ratos Sprague-Dawley , Tirosina 3-Mono-Oxigenase/genética , Tirosina 3-Mono-Oxigenase/metabolismo
10.
Hum Exp Toxicol ; 30(9): 1382-91, 2011 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-21081703

RESUMO

Paullinia cupana Mart. var. Sorbilis, commonly known as Guaraná, is a Brazilian plant frequently cited for its antioxidant properties and different pharmacological activities on the central nervous system. The potential beneficial uses of Guaraná in neurodegenerative disorders, such as in Parkinson's disease (PD), the pathogenesis of which is associated with mitochondrial dysfunction and oxidative stress, has not yet been assessed. Therefore, the main aim of the present study was to evaluate if an extract of commercial powdered seeds of Guaraná could protect human dopaminergic neuroblastoma SH-SY5Y cell line against rotenone-induced cytotoxicity. Two concentration of Guaraná dimethylsulfoxide extract (0.312 and 0.625 mg/mL) were added to SH-SY5Y cells treated with 300 nM rotenone for 48 h, and the cytoprotective effects were assessed by means of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, measuring lactate dehydrogenase (LDH) levels, and analyzing nuclear integrity with Hoechst33258 stain. Results showed that the addition of Guaraná extract significantly increased the cell viability of SH-SY5Y cells treated with rotenone, in a dose-dependent manner. On the other hand, LDH levels were significantly reduced by addition of 0.312 mg/mL of Guaraná, but unexpectedly, no changes were observed with the higher concentration. Moreover, chromatin condensation and nuclear fragmentation were significantly reduced by addition of any of both concentrations of the extract. The results obtained in this work could provide relevant information about the mechanisms underlying the degeneration of dopaminergic neurons in PD and precede in vivo experiments. Further studies are needed to investigate which active constituent is responsible for the cytoprotective effect produced by Paullinia cupana.


Assuntos
Antioxidantes/farmacologia , Inseticidas/toxicidade , Neurônios/efeitos dos fármacos , Paullinia/química , Extratos Vegetais/farmacologia , Rotenona/toxicidade , Técnicas de Cultura de Células , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Interpretação Estatística de Dados , Relação Dose-Resposta a Droga , Humanos , Neuroblastoma/patologia , Neurônios/patologia , Estresse Oxidativo/efeitos dos fármacos , Sementes/química
11.
Biochim Biophys Acta ; 1810(1): 93-110, 2011 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-20620191

RESUMO

BACKGROUND: The oxidoreductases of the thioredoxin (Trx) family of proteins play a major role in the cellular response to oxidative stress. Redox imbalance is a major feature of brain damage. For instance, neuronal damage and glial reaction induced by a hypoxic-ischemic episode is highly related to glutamate excitotoxicity, oxidative stress and mitochondrial dysfunction. Most animal models of hypoxia-ischemia in the central nervous system (CNS) use rats to study the mechanisms involved in neuronal cell death, however, no comprehensive study on the localization of the redox proteins in the rat CNS was available. METHODS: The aim of this work was to study the distribution of the following proteins of the thioredoxin and glutathione/glutaredoxin (Grx) systems in the rat CNS by immunohistochemistry: Trx1, Trx2, TrxR1, TrxR2, Txnip, Grx1, Grx2, Grx3, Grx5, and γ-GCS, peroxiredoxin 1 (Prx1), Prx2, Prx3, Prx4, Prx5, and Prx6. We have focused on areas most sensitive to a hypoxia-ischemic insult: Cerebellum, striatum, hippocampus, spinal cord, substantia nigra, cortex and retina. RESULTS AND CONCLUSIONS: Previous studies implied that these redox proteins may be distributed in most cell types and regions of the CNS. Here, we have observed several remarkable differences in both abundance and regional distribution that point to a complex interplay and crosstalk between the proteins of this family. GENERAL SIGNIFICANCE: We think that these data might be helpful to reveal new insights into the role of thiol redox pathways in the pathogenesis of hypoxia-ischemia insults and other disorders of the CNS. This article is part of a Special Issue entitled Human and Murine Redox Protein Atlases.


Assuntos
Sistema Nervoso Central/metabolismo , Glutarredoxinas/metabolismo , Tiorredoxinas/metabolismo , Animais , Atlas como Assunto , Sistema Nervoso Central/anatomia & histologia , Humanos , Hipóxia-Isquemia Encefálica/metabolismo , Hipóxia-Isquemia Encefálica/patologia , Imuno-Histoquímica , Masculino , Oxirredução , Ratos
12.
Rev. clín. med. fam ; 3(3): 237-239, oct. 2010. ilus
Artigo em Espanhol | IBECS | ID: ibc-84964

RESUMO

La meningitis carcinomatosa es una entidad poco frecuente, que puede formar parte de la historia natural de muchos procesos neoplásicos. Se presenta habitualmente con síntomas poco específicos, como cefalea, cambios en la conducta o alteraciones motoras y sensitivas. A continuación presentamos el caso de un paciente con carcinomatosis meníngea por cáncer de pulmón y su evolución clínica (AU)


Carcinomatis meningitis is a rare entity, which may be part of the natural history of many neoplasic. It usually present with nonspecific symptoms such as headache, changes in behavior or motor and sensory disturbances. We present the case of a patient with meningeal carcinomatosis from lung adenocarcinoma and its clinical evolution (AU)


Assuntos
Humanos , Masculino , Pessoa de Meia-Idade , Carcinoma/complicações , Carcinoma/diagnóstico , Meningite/complicações , Metástase Neoplásica/patologia , Metástase Neoplásica , Carcinoma/fisiopatologia , Carcinoma , Meningite , Crânio/patologia , Crânio
13.
Exp Neurol ; 223(2): 615-22, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-20206165

RESUMO

The capacity of the ovarian hormone 17beta-estradiol to prevent neurodegeneration has been characterized in several animal models of brain and spinal cord pathology. However, the potential reparative activity of the hormone under chronic neurodegenerative conditions has received less attention. In this study we have assessed the effect of estradiol therapy in adulthood on chronic glial and neuronal alterations caused by perinatal asphyxia (PA) in rats. Four-month-old male Sprague-Dawley rats submitted to PA just after delivery, and their control littermates, were injected for 3 consecutive days with 17beta estradiol or vehicle. Animals subjected to PA and treated with vehicle showed an increased astrogliosis, focal swelling and fragmented appearance of MAP-2 immunoreactive dendrites, decreased MAP-2 immunoreactivity and decreased phosphorylation of high and medium molecular weight neurofilaments in the hippocampus, compared to control animals. Estradiol therapy reversed these alterations. These findings indicate that estradiol is able to reduce, in adult animals, chronic reactive astrogliosis and neuronal alterations caused by an early developmental neurodegenerative event, suggesting that the hormone might induce reparative actions in the Central Nervous System (CNS).


Assuntos
Asfixia/tratamento farmacológico , Estradiol/farmacologia , Regeneração Nervosa/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Efeitos Tardios da Exposição Pré-Natal/tratamento farmacológico , Fatores Etários , Animais , Asfixia/patologia , Axônios/efeitos dos fármacos , Axônios/patologia , Região CA1 Hipocampal/efeitos dos fármacos , Região CA1 Hipocampal/patologia , Doença Crônica , Dendritos/efeitos dos fármacos , Dendritos/patologia , Feminino , Proteína Glial Fibrilar Ácida/metabolismo , Gliose/tratamento farmacológico , Gliose/patologia , Imuno-Histoquímica , Masculino , Proteínas Associadas aos Microtúbulos/metabolismo , Proteínas de Neurofilamentos/metabolismo , Neuroglia/metabolismo , Neuroglia/patologia , Neurônios/metabolismo , Neurônios/patologia , Neurônios/ultraestrutura , Gravidez , Efeitos Tardios da Exposição Pré-Natal/patologia , Ratos
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