RESUMEN

Objective: Although the prognosis of posterior reversible encephalopathy syndrome (PRES) is usually favourable and most patients wholly recover, the disorder can result in death in some patients. To date, the data on clinical features and risk factors for death are still lacking; therefore, we aim to investigate the clinical features and long-term prognostic risk factors of PRES in the present study. Methods: The patients with PRES were identified from the First Affiliated Hospital of Zhengzhou University from June 2011 to June 2020. Clinical characteristics, laboratory tests, magnetic resonance imaging examinations, and treatment of all patients were analyzed retrospectively. All patients were followed up by telephone. Finally, the patients were divided into the survival group and death group for prognosis analysis. Results: A total of 92 patients with PRES were included; 84.8% of whom were female, with an average age of 25.4 (5-66) years at the onset of PRES. Epilepsy was the main clinical manifestation (72.8%). The in-hospital mortality rate was 2.17%. The 3-year all-cause survival rate for PRES patients was 86%. In univariate analysis, patients with systemic lupus erythematosus (P = 0.027) and blood transfusion history within 1 month before onset (P = 0.027), need for dialysis (P ≤ 0.001), nephritis (P = 0.010), stroke (P = 0.016), and heart failure (P = 0.016) were associated with death. In multivariate analysis, we found that heart failure (OR = 0.095, 95% CI 0.020 to 0.441) and stroke (OR = 0.033, 95% CI 0.002 to 0.467) were independent risk factors for death in PRES patients, while pregnancy was a protective factor for death in PRES patients (OR = 7.978, 95% CI 1.446 to 44.006). Conclusions: Our results indicate that PRES could be considered as a sign of a very high-risk patient. We also demonstrated that heart failure and stroke were independent risk factors for death in patients with PRES; moreover, pregnancy was a protective factor.

Asunto(s)

Insuficiencia Cardíaca , Síndrome de Leucoencefalopatía Posterior , Accidente Cerebrovascular , Humanos , Femenino , Adulto , Masculino , Síndrome de Leucoencefalopatía Posterior/diagnóstico por imagen , Síndrome de Leucoencefalopatía Posterior/complicaciones , Estudios Retrospectivos , Factores de Riesgo , Accidente Cerebrovascular/complicaciones

RESUMEN

Epilepsy is a common neurological disorder in the central nervous system. Inflammation disrupts the blood-brain barrier (BBB), which is responsible for maintaining brain homeostasis. This study was aimed to investigate the functional role of microRNA (miR)-132 in hippocampal HT-22 cells under lipopolysaccharide (LPS) stimulation. In vitro cell inflammatory model was constructed by LPS stimulation. Inflammatory cell injury was evaluated according to the alterations of cell viability, apoptosis, and expression of inflammatory cytokines. Then, miR-132 level after LPS treatment was assessed. Subsequently, miR-132 was abnormally expressed after cell transfection, and the effects of miR-132 on LPS-induced cell inflammatory injury as well as phosphorylated levels of key kinases in the NF-κB and MAPK kinase (MEK)/ERK pathways were determined. The target gene of miR-132 was virtually screened and verified, and whether miR-132 affected HT-22 cells under LPS stimulation through regulating the target gene was verified. The results showed that the level of miR-132 was down-regulated by LPS in HT-22 cells, and the LPS-induced inflammatory injury could be reduced by miR-132 overexpression. Then, the phosphorylated levels of kinases in the NF-κB and MEK/ERK pathways were decreased by miR-132 overexpression. Tumor necrosis factor receptor-associated factor 6 (TRAF6) was predicted and verified to be a target of miR-132. Moreover, the alterations induced by miR-132 overexpression in the LPS-treated HT-22 cells were abrogated by TRAF6 overexpression. Therefore, we drew the conclusion that LPS down-regulated miR-132 and miR-132 attenuated LPS-induced inflammatory cell injury by targeting TRAF6, along with the inhibition of the NF-κB and MEK/ERK pathways.

Asunto(s)

Inflamación/prevención & control , MicroARNs/genética , Neuronas/efectos de los fármacos , Factor 6 Asociado a Receptor de TNF/metabolismo , Animales , Apoptosis , Supervivencia Celular , Células Cultivadas , Citocinas , Inflamación/inducido químicamente , Inflamación/genética , Lipopolisacáridos/toxicidad , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Ratones , FN-kappa B/genética , FN-kappa B/metabolismo , Neuronas/inmunología , Neuronas/metabolismo , Fosforilación , Transducción de Señal , Factor 6 Asociado a Receptor de TNF/genética

Asunto(s)

Intoxicación por Mercurio , Preparaciones para Aclaramiento de la Piel/envenenamiento , Adulto , Humanos , Mercurio , Persona de Mediana Edad

RESUMEN

BACKGROUND: The etiology and pathogenesis of bronchial asthma remain unclear. This study is to investigate the risk factors related to bronchial asthma onset in children from genetics and immunology and preliminarily reveal the pathogenesis of bronchial asthma in children. METHODS: Real-time quantitative PCR was adopted to detect the expression level of TRPV1 gene and mRNA and enzyme-linked immunosorbent assay method to the total immunoglobulin E level and levels of IL-4, IL-5, and IFN-γ in serum in peripheral venous blood for children in two groups. Logistic regression analysis was applied to analyze the most essential factors inducing bronchial asthma in children. RESULTS: The mRNA level of TRPV1 in peripheral blood in the case group was higher than that in the control group (P < 0.01). The levels of IL-4, IL-5, and eosinophils in serum in the case group were markedly higher than those in the control group (P < 0.01), while IFN-γ level in the case group was lower than that in the control group (P < 0.01). The results of logistic regression analysis indicated that TRPV1 expression level, IL-4 level, and rs4790522 site mutation were the main risk factors inducing bronchial asthma in children. CONCLUSION: The levels of TRPV1 gene expression and Th1/Th2 cytokines have a close relationship with asthma onset in children, which provides theoretical evidences for molecular targeted treatment in children with bronchial asthma.

Asunto(s)

Asma/genética , Asma/inmunología , Asma/fisiopatología , Polimorfismo de Nucleótido Simple , Canales Catiónicos TRPV/metabolismo , Alelos , Estudios de Casos y Controles , Niño , Preescolar , Ensayo de Inmunoadsorción Enzimática , Eosinófilos/metabolismo , Femenino , Humanos , Interferón gamma/sangre , Interleucina-4/sangre , Interleucina-5/sangre , Masculino , Mutación , Reacción en Cadena en Tiempo Real de la Polimerasa , Análisis de Regresión , Factores de Riesgo , Canales Catiónicos TRPV/genética

Asunto(s)

Errores Innatos del Metabolismo de los Aminoácidos/complicaciones , Errores Innatos del Metabolismo de los Aminoácidos/psicología , Homocistinuria/complicaciones , Homocistinuria/psicología , Trastornos Mentales/etiología , Trastornos Mentales/psicología , Vitamina B 12/sangre , Adolescente , Adulto , Errores Innatos del Metabolismo de los Aminoácidos/sangre , Niño , Electromiografía , Femenino , Estudios de Seguimiento , Homocistinuria/sangre , Humanos , Imagen por Resonancia Magnética , Masculino , Vitamina B 12/análogos & derivados , Vitamina B 12/uso terapéutico , Deficiencia de Vitamina B 12/congénito , Vitaminas/uso terapéutico , Adulto Joven

RESUMEN

OBJECTIVES: To investigate the protective effect of catalpol on cerebral ischaemia/reperfusion (CI/R) injury in gerbils and further explore the underlying mechanism. METHODS: A gerbil model of CI/R was prepared by bilateral common carotid occlusion for 10 min followed by 6 h reperfusion. Catalpol (5, 10 or 20 mg/kg per day) was injected intraperitoneally for 3 days before the carotid occlusion. Stroke index was measured during the reperfusion. The contents of endogenous neuropeptides, endothelin-1 (ET-1) and calcitonin gene-related peptide in plasma were evaluated by radioimmunoassay. Superoxide dismutase (SOD) and malondialdehyde (MDA) in brain tissue homogenate were also examined. KEY FINDINGS: The results showed that catalpol significantly improved the stroke index compared with CI/R control group (P < 0.05 or P < 0.01). Catalpol significantly increased the activity of SOD at the doses of 10 and 20 mg/kg (P ≤ 0.05), decreased the brain MDA content and the plasma level of ET-1 at the doses of 10 and 20 mg/kg (P ≤ 0.01). CONCLUSIONS: These data suggested that the efficacy of catalpol pretreatment on CI/R injury may be attributed to reduction of free radicals and inhibition of lipid peroxidation and ET-1 production.

Asunto(s)

Isquemia Encefálica/tratamiento farmacológico , Encéfalo/efectos de los fármacos , Infarto Cerebral/tratamiento farmacológico , Glucósidos Iridoides/uso terapéutico , Fitoterapia , Daño por Reperfusión/prevención & control , Accidente Cerebrovascular/prevención & control , Animales , Encéfalo/metabolismo , Isquemia Encefálica/metabolismo , Péptido Relacionado con Gen de Calcitonina/sangre , Infarto Cerebral/metabolismo , Modelos Animales de Enfermedad , Endotelina-1/sangre , Femenino , Radicales Libres/metabolismo , Gerbillinae , Inyecciones Intraperitoneales , Glucósidos Iridoides/farmacología , Peroxidación de Lípido/efectos de los fármacos , Masculino , Malondialdehído/metabolismo , Neuropéptidos/metabolismo , Estrés Oxidativo/efectos de los fármacos , Extractos Vegetales/farmacología , Extractos Vegetales/uso terapéutico , Rehmannia/química , Daño por Reperfusión/sangre , Daño por Reperfusión/metabolismo , Superóxido Dismutasa/metabolismo

RESUMEN

Resveratrol is a natural polyphenol widely present in plants, particularly in the skin of red grapes and in wine. It possesses a wide range of biological effects and exhibits neuroprotective effects in numerous diseases. However, data evaluating the effects of resveratrol in vascular dementia (VaD) are lacking. In the present study, the permanent, bilateral common carotid artery occlusion rat model was used to study the effects of resveratrol on VaD. The Morris water maze was used to test the spatial learning and memory performance of the rats. The expression levels of Bax, Bcl-2, cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP) in the hippocampus were measured. The results showed that resveratrol inhibited memory impairment in the VaD rat model, and attenuated the increases in the expression levels of Bax, cleaved caspase-3 and cleaved PARP and the reductions in the expression levels of Bcl-2 that were induced by VaD. These results provide a novel insight into the neuroprotective effects of resveratrol and its possible therapeutic role in VaD.

RESUMEN

This study aimed to investigate the effects of catalpol on ATPase and amino acids in gerbils following cerebral ischemia/reperfusion (CI/R) injury. Gerbil model of CI/R was prepared by bilateral common carotid occlusion for 10 min followed by 6 h of reperfusion. Catalpol (5, 10 or 20 mg/kg per day) was injected intraperitoneally for 3 days before the carotid occlusion. Stroke index was measured during the reperfusion. ATPase activity, glutamate (Glu) and aspartate contents in brain tissue homogenate were examined. The results showed that catalpol significantly improved the stroke index compared with sham group (P < 0.05 or P < 0.01). Catalpol markedly increased the activities of Na(+)-K(+)-ATPase and Ca(2+)-ATPase (P < 0.05 or P < 0.01), and significantly decreased the content of Glu in brain tissue (P < 0.05 or P < 0.01). These data suggest that the efficacy of catalpol pretreatment on CI/R injury is associated with the enhancement of ATPase activity and the inhibition of excitatory amino acid toxicity.

Asunto(s)

Adenosina Trifosfatasas/análisis , Ácido Aspártico/análisis , Química Encefálica/efectos de los fármacos , Isquemia Encefálica/tratamiento farmacológico , Ácido Glutámico/análisis , Glucósidos Iridoides/uso terapéutico , Proteínas del Tejido Nervioso/análisis , Fármacos Neuroprotectores/uso terapéutico , Daño por Reperfusión/tratamiento farmacológico , Animales , Isquemia Encefálica/metabolismo , Arteria Carótida Común , Membrana Celular/enzimología , Constricción , Relación Dosis-Respuesta a Droga , Evaluación Preclínica de Medicamentos , Femenino , Gerbillinae , Glucósidos Iridoides/administración & dosificación , Glucósidos Iridoides/química , Glucósidos Iridoides/farmacología , Masculino , Modelos Animales , Estructura Molecular , Fármacos Neuroprotectores/administración & dosificación , Fármacos Neuroprotectores/química , Fármacos Neuroprotectores/farmacología , Premedicación , Daño por Reperfusión/metabolismo , Método Simple Ciego

RESUMEN

Cerebral ischemia is the main cause of cognitive impairment. Changes in dendritic morphology and spines have been shown to occur with synaptic plasticity and cognitive function. Bilateral occlusion of the common carotid arteries (2VO) in rats was an effective model of chronic cerebral ischemia. In this experiment, SD rats were divided into model group (2VO) and sham-operated group. At 2, 4, 8 and 16 weeks, rats were tested in Morris water maze to observe learning and memory abilities, and then the brain tissue was stained by Golgi method to investigate the morphology of dendrites of pyramidal neurons under light microscope. Dendritic length and arborization and spine density of pyramidal neurons in medial prefrontal cortex (mPFC) and hippocampal CA1 were analyzed by ImageJ. Progressive learning and memory deficits appeared since 2 weeks. Compared to the sham-operated group, the dendritic length and arborization significantly decreased in the model group at 4, 8 and 16 weeks after 2VO in CA1, while there was no significant difference in mPFC. Dendritic spine density in hippocampal CA1 of the model group significantly decreased after 2 weeks, and it was decreased after 8 weeks in mPFC. The results suggest that under the condition of chronic cerebral ischemia, the alteration of dendritic morphology and spine density underlay cognitive impairment.

Asunto(s)

Isquemia Encefálica/patología , Dendritas/ultraestructura , Hipocampo/ultraestructura , Corteza Prefrontal/ultraestructura , Animales , Modelos Animales de Enfermedad , Aprendizaje por Laberinto/fisiología , Neuronas/ultraestructura , Ratas , Ratas Sprague-Dawley

RESUMEN

Wernicke's encephalopathy (WE) is a severe neurological disorder caused by thiamine deficiency. Clinically, it is most frequently observed in people with alcohol abuse. WE, however, can occur in any clinical condition associated with malnutrition or thiamine deficiency. We present the case of a 47-year-old woman with prolonged therapeutic fasting who presented with ophthalmoplegia, ataxia and deep coma. MRI showed unusual symmetric cortical abnormalities in the frontal and parietal lobes, as well as typical lesions surrounding the third ventricle and aqueduct. Although the patient entered a vegetative state, she finally regained consciousness after thiamine supplementation unexpectedly. To the best of our knowledge, it has never been reported to date that the patient with WE in a vegetative state with cortical damage shows a marvelous prognosis, which prompts us to report this case. In the present report, we highlight the role of MRI in the diagnosis of acute WE.

Asunto(s)

Pancreatitis/complicaciones , Encefalopatía de Wernicke/diagnóstico , Encefalopatía de Wernicke/etiología , Imagen de Difusión por Resonancia Magnética , Femenino , Humanos , Persona de Mediana Edad , Lóbulo Parietal/patología , Sustancia Gris Periacueductal/patología , Tálamo/patología

RESUMEN

OBJECTIVE: To investigate the protective effects of musk extract (ME) and its possible mechanism on rat's cerebral cortical neurons with inflammatory injury induced by lipopolysaccharide (LPS). METHODS: Neurons and astrocytes from newborn rat cerebral cortex were cultured in vitro respectively, and the astrocyte conditioned medium (ACM), obtained by treating astrocytes with 10 mg/L LPS and different concentrations of ME for 24 h, was added in the culture fluid of neurons. The survival rate and apoptotic rate of neurons were measured by MTT method and AO/EB stain; and the changes of inflammatory factors in the ACM were determined by ELISA. RESULTS: The survival rate (%) of neurons treated by ACM with ME in concentrations of 18 mg/L, 36 mg/L, 72 mg/L and 144 mg/L was 52.55 +/- 3.52, 55.77 +/- 2.36, 64.89 +/- 3.45 and 73.67 +/- 1.80, respectively, significantly higher than that in the model neurons (43.62 +/- 4. 51, P < 0.05), while the apoptotic rate (%) in them, 68.11 +/- 2.16, 44.27 +/- 3.68, 32.56 +/- 2.14 and 21.89 +/- 2.46, respectively, was significantly lower than that in model neurons (71.33 +/- 3.25, P < 0.05 or P < 0.01). Level of IL-6 was decreasing along with the raising of ME concentration in the ACM, showing a concentration-dependent state. CONCLUSION: ME shows apparent protective effect on neurons against inflammatory injury, especially in a high concentration (144 mg/L), which may be associated with the reduction of IL-6 secreted by astrocytes.

Asunto(s)

Corteza Cerebral/citología , Ácidos Grasos Monoinsaturados/química , Inflamación/prevención & control , Neuronas/citología , Sustancias Protectoras/farmacología , Animales , Animales Recién Nacidos , Astrocitos/citología , Astrocitos/metabolismo , Supervivencia Celular/efectos de los fármacos , Células Cultivadas , Inflamación/inducido químicamente , Interleucina-6/metabolismo , Lipopolisacáridos , Masculino , Materia Medica/farmacología , Ratas , Ratas Wistar

RESUMEN

OBJECTIVE: To study the changes of microRNA expression in cortex tissues in neonatal rats with hypoxic-ischemic brain damage (HIBD)and the possible roles of microRNA in the pathogenesis of HIBD. METHODS Rat HIBD model was prepared. The cortex tissues were obtained 14 days after the HIBD event. The microRNA expression profiles were measured using microRNA microarray. Expression of 9 microRNAs (miR-126,-26a,-674-5p,-21,-25,-290, miR-124,-125b-5p and microRNA-9a) was determined by quantitative real-time PCR. RESULTS: he results of microRNA expression profiles indicated that 27 pieces of microRNA were up-regulated more than 2 folds and 60 pieces were down-regulated more than 2 folds compared with the normal control group. The results of the 9 microRNAs detected by quantitative real-time PCR were consistent with those detected by microRNA microarray. CONCLUSIONS: HIBD rats have significant changes in microRNA expression, suggesting that microRNA expression may play important roles in the pathogenesis of HIBD.

Asunto(s)

Hipoxia-Isquemia Encefálica/genética , MicroARNs/fisiología , Animales , Animales Recién Nacidos , Apoptosis , Ciclo Celular , Hipoxia-Isquemia Encefálica/etiología , MicroARNs/genética , Análisis de Secuencia por Matrices de Oligonucleótidos , Reacción en Cadena de la Polimerasa , Ratas , Ratas Sprague-Dawley

RESUMEN

OBJECTIVE: To study the effects of Down syndrome cellular adhesion molecule (DSCAM) on differentiation of rat marrow mesenchymal stem cells (MSCs) into neurons in vitro. METHODS: MSCs from Sprague-Dawley rats were induced into neurons by baicalin. The expression of DSCAM before and after induction was evaluated by immunocytochemical staining and Western blot assay. After knockdown of DSCAM by siRNA transfection, the differentiation rate of neurons derived from MSCs was measured. RESULTS: Before induction, the expression of DSCAM was not detectable in MSCs. After bFGF preinduction for 24 hrs, DSCAM was slightly expressed in MSCs (1.71+/- 0.67%). The DSCAM expression increased 6 hrs after baicalin induction (15.79+/- 4.24%), reached a peak at 3 days (53.16+/- 5.94%) and then decreased gradually. The DSCAM expression 6 days after baicalin induction (28.99+/- 6.72%) was significantly lower than that at 3 days (P<0.01). However, after DSCAM-siRNA transfection, the DSCAM expression in MSCs was significantly reduced. MSCs did not express neuron-specific beta-III-tubulin before induction. After baicalin induction for 6 hrs, 3 days and 6 days, the expression of beta-III-tubulin was 1.40+/- 0.79%, 41.59+/- 3.17% and 59.11+/- 4.76% respectively. But the beta-III-tubulin expression significantly decreased 3 and 6 days after DSCAM-siRNA transfection (28.57+/- 2.91% and 43.90+/- 12.31% respectively). CONCLUSIONS: DSCAM may play an important role in MSCs differentiation into neural cells.

Asunto(s)

Células de la Médula Ósea/citología , Moléculas de Adhesión Celular/fisiología , Diferenciación Celular , Células Madre Mesenquimatosas/citología , Neuronas/citología , Animales , ARN Interferente Pequeño/genética , Ratas , Ratas Sprague-Dawley , Transfección

RESUMEN

OBJECTIVE: To investigate the role of Notch-1 signaling in bone marrow mesenchymal stem cells (MSCs) differentiating into neurons. METHODS: Mice Notch-1 small hairpin RNA (mNotch-1 shRNA) was constructed and transfected into the MSCs obtained from the tibiae of BALB/c mice. MSCs transfected with glyceraldehyde-3-phosphate hydoxygenase (GADPH) shRNA and untransfected MSCs were used as controls. The cell survival rate was detected by ELISA. The MSCs of different groups were cultured in Neurobasal-A medium so as to be induced to differentiate into neurons. Apoptosis of the MSCs was detected by TUNEL. RESULTS: After induction of 6 days the MSCs transfected with mNotch-1 shRNA displayed typical neuronal morphology and high expression of neuron-specific markers: nestin, neuron-specific enolase (NSE), neurofilament 200 (NF 200), and Notch-1 protein, however, gilal fibrillary acidic protein (GFAP), the glia-specific marker, was not detected. The percentage of apoptotic cells in the MSCs transfected with mNotch-1 shRNA was 13.3% +/- 2.3%, significantly higher than those of the MSCs transfected with mGAPH shRNA and untransfected MSCs (4.7% +/- 0.5% and 4.5% +/- 0.4%, both P < 0.01). CONCLUSION: Block of the Notch signal pathway may increase the differentiation of MSCs into neurons.

Asunto(s)

Células de la Médula Ósea/citología , Diferenciación Celular/fisiología , Neuronas/citología , Receptor Notch1/fisiología , Animales , Apoptosis/genética , Apoptosis/fisiología , Western Blotting , Células de la Médula Ósea/metabolismo , Diferenciación Celular/genética , Supervivencia Celular/genética , Supervivencia Celular/fisiología , Femenino , Proteína Ácida Fibrilar de la Glía/análisis , Inmunohistoquímica , Etiquetado Corte-Fin in Situ , Masculino , Ratones , Ratones Endogámicos BALB C , Proteínas de Neurofilamentos/análisis , Neuronas/metabolismo , ARN Interferente Pequeño/genética , Receptor Notch1/genética , Receptor Notch1/metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Transfección