RESUMEN
Flocculent is commonly used in mining activities to improve the concentration of tailing slurry by enhancing the sedimentation process of small tailings particles. The presence of flocculent in thickened tailings is unavoidable, and it affects the heavy metal leaching performances and mechanical and rheological characteristics of tailing-based cemented paste backfill (CPB). This study is carried out to investigate the physicochemical and leachability of CPB amended with flocculants and lime-activated ground granulated blast-furnace slag (GGBS). The stabilized samples were subjected to a series of model tests, including toxicity characteristics leaching procedure (TCLP) and pH, unconfined compressive strength (UCS), scanning electron microscopy (SEM), and X-ray diffraction. Moreover, the CPB amended with anionic polyacrylamide (APAM) demonstrated better performance in terms of a decrease in heavy metal leachability besides higher mechanical strength than poly aluminum chloride (PAC) and poly ferric chloride (PFC) samples. Furthermore, the UCS results showed that increasing binder content up to 15% negatively influences strength improvement of all stabilized samples because of weak connections between soil particles and cementitious material, resulting in high leachability of heavy metals. The analysis of XRD and SEM showed that anionic polyacrylamide (APAM) cases exhibited more voluminous hydration products, resulting in a compact stabilized matrix and substantially reduced heavy metal leachability.
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Metales Pesados , Agua , Agua/química , Óxidos/química , Compuestos de Calcio/química , Metales Pesados/análisisRESUMEN
BACKGROUND: Parkinson's disease is a common neurodegenerative problem. Pramipexole (PPX) plays protective role in Parkinson's disease. Nevertheless, the mechanism of PPX in Parkinson's disease-like neuronal injury is largely uncertain. METHODS: 1-methyl-4-phenylpyridinium (MPP+)-stimulated neuronal cells and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mice were used as the model of Parkinson's disease. MPP+-induced neuronal injury was assessed via cell viability, lactic dehydrogenase (LDH) release and apoptosis. microRNA-96 (miR-96) and BCL2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3) abundances were examined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or Western blotting. Mitophagy was tested by Western blotting and immunofluorescence staining. MPTP-induced neuronal injury in mice was investigated via behavioral tests and TUNEL. RESULTS: PPX alleviated MPP+-induced neuronal injury via increasing cell viability and decreasing LDH release and apoptosis. PPX reversed MPP+-induced miR-96 expression and inhibition of mitophagy. miR-96 overexpression or BNIP3 interference weakened the suppressive role of PPX in MPP+-induced neuronal injury. miR-96 targeted BNIP3 to inhibit PTEN-induced putative kinase 1 (PINK1)/Parkin signals-mediated mitophagy. miR-96 overexpression promoted MPP+-induced neuronal injury via decreasing BNIP3. PPX weakened MPTP-induced neuronal injury in mice via regulating miR-96/BNIP3-mediated mitophagy. CONCLUSION: PPX mitigated neuronal injury in MPP+-induced cells and MPTP-induced mice by activating BNIP3-mediated mitophagy via directly decreasing miR-96.
Asunto(s)
Antiparkinsonianos/administración & dosificación , Proteínas de la Membrana/metabolismo , MicroARNs/metabolismo , Proteínas Mitocondriales/metabolismo , Mitofagia/efectos de los fármacos , Trastornos Parkinsonianos/metabolismo , Pramipexol/administración & dosificación , Animales , Línea Celular Tumoral , Relación Dosis-Respuesta a Droga , Humanos , Masculino , Ratones , Ratones Endogámicos C57BL , MicroARNs/antagonistas & inhibidores , Mitofagia/fisiología , Neuronas/efectos de los fármacos , Neuronas/metabolismo , Trastornos Parkinsonianos/inducido químicamente , Trastornos Parkinsonianos/tratamiento farmacológicoRESUMEN
Willed-movement training has been demonstrated to be a promising approach to increase motor performance and neural plasticity in ischemic rats. However, little is known regarding the molecular signals that are involved in neural plasticity following willed-movement training. To investigate the potential signals related to neural plasticity following willed-movement training, littermate rats were randomly assigned into three groups: middle cerebral artery occlusion, environmental modification, and willed-movement training. The infarct volume was measured 18 d after occlusion of the right middle cerebral artery. Reverse transcription-polymerase chain reaction (PCR) and immunofluorescence staining were used to detect the changes in the signal transducer and activator of transcription 3 (STAT3) mRNA and protein, respectively. A chromatin immunoprecipitation was used to investigate whether STAT3 bound to plasticity-related genes, such as brain-derived neurotrophic factor (BDNF), synaptophysin, and protein interacting with C kinase 1 (PICK1). In this study, we demonstrated that STAT3 mRNA and protein were markedly increased following 15-d willed-movement training in the ischemic hemispheres of the treated rats. STAT3 bound to BDNF, PICK1, and synaptophysin promoters in the neocortical cells of rats. These data suggest that the increased STAT3 levels after willed-movement training might play critical roles in the neural plasticity by directly regulating plasticity-related genes.
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Isquemia Encefálica/rehabilitación , Terapia por Ejercicio/métodos , Plasticidad Neuronal/fisiología , Factor de Transcripción STAT3/fisiología , Transducción de Señal , Animales , Isquemia Encefálica/fisiopatología , Factor Neurotrófico Derivado del Encéfalo/metabolismo , Proteínas Portadoras/metabolismo , Proteínas del Citoesqueleto , Masculino , Actividad Motora , Proteínas Nucleares/metabolismo , ARN Mensajero/análisis , Ratas , Ratas Sprague-Dawley , Factor de Transcripción STAT3/genéticaRESUMEN
OBJECTIVES: Chronic cerebral hypoperfusion (CCH) leads to neurodegeneration and cognitive impairment. Ubiquitinated protein aggregates are commonly present in neurodegenerative disorders and are believed to cause neuronal degeneration. Here, we investigated the effects of N-stearoyl-L-tyrosine (NSTyr) on the hippocampal ubiquitin-proteasome system (UPS) in rats with CCH. METHODS: After induction of CCH, NSTyr was intraperitoneally administered daily for 3 months. Protein aggregation was analyzed by ethanolic phosphotungstic acid (EPTA) electron microscopy (EM), immunogold EM, laser-scanning confocal microscopy, and Western blot. Proteasome peptidase activity was measured by peptidase activity assays. RESULTS: By using EPTA EM, immunogold EM and high-resolution laser-scanning confocal microscopy, we found that CCH resulted in the accumulation of ubiquitinated protein aggregates in rat hippocampal CA1 neurons. Western blot revealed that the levels of free ubiquitin were significantly reduced and that the levels of ubiquitinated proteins were markedly increased in the hippocampus of CCH rats. Direct activity measurements demonstrated that proteasome peptidase activity in the hippocampal region of rats was decreased after CCH induction. In the hippocampal tissue of CCH rats treated with NSTyr, however, ubiquitinated protein aggregates decreased and proteasome peptidase activity increased. DISCUSSION: These data indicate that NSTyr may exert protective effects on rat hippocampal UPS function via endogenous regulation.
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Región CA1 Hipocampal/metabolismo , Corteza Cerebral/irrigación sanguínea , Complejo de la Endopetidasa Proteasomal/metabolismo , Tirosina/análogos & derivados , Ubiquitina/metabolismo , Animales , Región CA1 Hipocampal/citología , Región CA1 Hipocampal/efectos de los fármacos , Neuronas/citología , Neuronas/metabolismo , Ratas , Ratas Sprague-Dawley , Tirosina/farmacologíaRESUMEN
OBJECTIVE: To explore the methods for identification of sibling brothers with Y-STR locus mutation by detection of genetic markers on autosome and Y-biallelic. METHODS: Goldeneye 20A and 18NC kit were used to genotyped the 35 STRs on autosome from two men. PowerPlex Y kit and Yfiler kit were used to genotyped the 16 STRs on Y chromosome full sibling index was calculated by ITO method. Twenty Y-biallelic markers were genotyped by fragment length discrepant allele specific PCR or general PCR. RESULTS: Relationship of sibling brothers was found to have mutation of 2 loci on 16 Y-STR and the identical genetype of 20 Y-biallelic markers as well as a cumulative full sibling index of 4.3149 x 10(6) from 35 STRs on autosome. CONCLUSION: In identification of paternal linage of Y-STR mutation, more genetic information can be acquired by detection of Y-biallelic markers including SNP and InDel.
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Alelos , Cromosomas Humanos Y/genética , Repeticiones de Microsatélite/genética , Hermanos , Genética Forense/métodos , Frecuencia de los Genes , Sitios Genéticos/genética , Marcadores Genéticos , Genotipo , Humanos , Masculino , Mutación , Reacción en Cadena de la Polimerasa/métodos , Polimorfismo GenéticoRESUMEN
OBJECTIVE: To investigate the relationship between C923T (Ala308Val) polymorphism in exon 10 of protein 47000 phagocyte oxidase(p47(phox)) gene and stroke and to evaluate the effect of C923T (Ala308Val) polymorphism on plasma lipid levels in Hunan Hans population. METHODS: Hunan Han population C923T (Ala308Val) polymorphism in p47phox gene was determined by PCR-single strand conformation polymorphism analysis and DNA sequencing in 100 healthy controls, 220 patients with stroke, and 10 stroke pedigrees. Plasma lipid levels were measured by routine methods. RESULTS: No statistically significant differences were found in frequencies of genotypes and alleles of C923T (Ala308Val) polymorphism between the controls and stroke patients (P > 0.05). The serum levels of triglyceride in cerebral infarction patients and controls with CT genotype were markedly higher than those with CC genotype (P < 0.05). CONCLUSION: There is no association between C923T (Ala308Val) polymorphism and stroke in Hunan Hans; C923T (Ala308Val) polymorphism is associated with plasma lipid metabolism in Hunan Han population with cerebral infarction.
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Exones/genética , Lípidos/sangre , NADPH Oxidasas/genética , Polimorfismo de Nucleótido Simple , Accidente Cerebrovascular/sangre , Accidente Cerebrovascular/genética , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Secuencia de Bases , Estudios de Casos y Controles , Etnicidad/genética , Femenino , Frecuencia de los Genes , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo Conformacional Retorcido-SimpleRESUMEN
OBJECTIVE: To investigate the relationship between C923T (Ala308Val) polymorphism in the exon10 of P47(phox) gene and cerebral infarction and to evaluate the effect of C923T polymorphism on plasma lipid levels. METHODS: Peripheral blood samples were collected from 110 patients with cerebral infarction, 100 sex and age-matched healthy controls, and 102 members of 10 cerebral infarction pedigrees 19 of which were cerebral infarction patients. The polymorphism in P47(phox) gene was determined by PCR-single strand conformation polymorphism analysis and DNA sequencing. Plasma lipid levels were measured by routine methods. RESULTS: Three gene types, CC, CT, and TT were found in the C923T (Ala308Val) polymorphism site. No statistically significant differences were found in the frequencies of genotypes and alleles of C923T polymorphism between the controls and cerebral infarction patients (all P > 0.05). The serum levels of triglyceride of cerebral infarction patients and controls with the CT genotype were markedly higher than those of the cerebral infarction patients and controls with the CC genotype (both P < 0.05). CONCLUSION: There is no association between the C923T polymorphism and cerebral infarction. C923Tpolymorphism is associated with plasma lipid metabolism.
Asunto(s)
Infarto Cerebral/patología , Lípidos/sangre , NADPH Oxidasas/genética , Polimorfismo Genético , Adolescente , Adulto , Anciano , Apolipoproteína A-I/sangre , Secuencia de Bases , Infarto Cerebral/sangre , Infarto Cerebral/genética , Colesterol/sangre , HDL-Colesterol/sangre , LDL-Colesterol/sangre , Femenino , Frecuencia de los Genes , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Triglicéridos/sangre , Adulto JovenRESUMEN
BACKGROUND AND PURPOSE: Cognitive deficits after stroke are common and interfere with recovery. One purpose of this study was to determine whether the motor abilities of subjects who have poststroke cognitive deficits and who have received problem-oriented willed-movement (POWM) therapy will improve more than the motor abilities of subjects in the reference group who have received neurodevelopmental treatment (NDT). Another purpose of this study was to identify the relationship between cognitive function and motor abilities for both groups. SUBJECTS: The subjects recruited for this study were 36 men and 11 women with various degrees of poststroke cognitive deficits. METHODS: A randomized block design was used to assign the subjects to 2 groups. Cognitive function and motor ability were evaluated with the Mini-Mental State Examination and the Stroke Rehabilitation Assessment of Movement (STREAM). Both groups received physical therapy 5 or 6 times per week in 50-minute sessions. RESULTS: The STREAM scores improved after treatment in both groups. Main group effects were found for the lower-extremity (F=4.58, P< .05) and basic mobility (F=27.49, P< .01) subscales of the STREAM. Pretest cognitive function showed a positive relationship with posttest motor ability in the NDT group (r = .446, P< .05). However, the relationship between pretest cognitive function and posttest motor ability had no statistical significance in the POWM group (r = .101, P= .630). DISCUSSION AND CONCLUSION: These findings suggest that, regardless of a person's cognitive function, POWM intervention is effective in improving lower-extremity and basic mobilities and indicates the need to use relatively intact cognitive function or perceptual function, or both, to improve motor rehabilitation for people with cognitive function deficits.
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Trastornos del Conocimiento/rehabilitación , Personas con Discapacidad/rehabilitación , Destreza Motora , Modalidades de Fisioterapia/normas , Rehabilitación de Accidente Cerebrovascular , Volición , Adulto , Anciano , China , Trastornos del Conocimiento/etiología , Femenino , Estudios de Seguimiento , Humanos , Locomoción , Masculino , Persona de Mediana Edad , Recuperación de la Función , Índice de Severidad de la Enfermedad , Accidente Cerebrovascular/complicaciones , Factores de TiempoRESUMEN
OBJECTIVE: To explore the function of CD62p in cerebral infarction and the relation between the changes of its level and the severity and recovery of cerebral infarction, MPV, PDW and PLT by studying the changes of the levels of plasma CD62p in patients with acute cerebral infarction. METHODS: The levels of plasma CD62p were measured by ELISA in 60 patients at 48 hours, 6 - 8 days and 15 days after ischemia, and at the same time, we evaluated neurological function deficiency score and measured MPV, PDW and PLT. The levels of 30 healthy persons mating cerebral infarction group in both sex and ages were measured. RESULTS: The levels of plasma CD62p in the patients with acute cerebral infarction were obviously higher than the levels of the healthy controls (P < 0.001). The levels of plasma CD62 p in CI group at 48 hours postischemia were higher than the levels at 6 - 8 days and at 15 days with obvious difference (P <0.01). The levels of plasma CD62p in the medium and the severe SSS patients were higher than the levels of the lights (P <0.001). The levels of plasma CD62p were positively correlated with SSS, MPV and PDW (r = 0.61, 0.51, 0.47, P < 0.01), and negatively correlated with PLT (r = -0.32, P < 0.01). CONCLUSION: CD62p may participate in acute cerebral infarction and play a crucial role, and the change of its levels correlates with SSS, MPV, PDW and Plt.
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Infarto Cerebral/sangre , Selectina-P/sangre , Adulto , Anciano , Anciano de 80 o más Años , Ensayo de Inmunoadsorción Enzimática , Femenino , Humanos , Masculino , Persona de Mediana Edad , PronósticoRESUMEN
OBJECTIVE: To analyze the changes and clinical significance of IL-6 and sICAM-1, and to explore their pathologic mechanism in the brain ischemia. METHODS: Thirty-two patients at Xiangya Hospital who experienced infarcts that occurred within the first 3 days were consecutively selected into the study, and 30 healthy subjects were selected as controls. The serum level of IL-6 and sICAM-1 was measured by radioimmunoassy and enzyme linked immunosorbent assay. Eleven out of the 32 patients that experienced stroke within 24 hours were observed on the 1st, 3rd, and 6th day. The subsequent volume of brain lesion as a consequence of stroke was measured by CT within 48 - 72 hours after the onset. RESULTS: Both the serum levels of IL-6 and sICAM-1 were significantly higher in patients within the first 3 days after the onset than those of the controls [(352. 1 +/- 31.7) pg/ml vs. (135.4 +/- 18.3) pg/ml, and (363.6 +/- 48.4) ng/ml vs. (227.2 +/- 30.1) ng/ml, P < 0.01]. The levels of IL-6 at the 6th day [(308.3 +/- 26.8) pg/ml] was significantly lower than that both on the 1st day [(364.5 +/- 29.7) pg/ml] and on the 3rd day [(345 +/- 28.9) pg/ml] (P <0.01). There was no significant difference between the 1st day and the 3rd day (P > 0.05). Statistical significance existed in each two concentrations of sICAM-1 on the 1st day [(383.9 +/- 56.1) ng/ml], the 3rd day [(354.6 +/- 40.8) ng/ml], and the 6th day [(316.7 +/- 32.3) ng/ml] (P < 0.05). Both the levels of IL-6 and sICAM-1 were higher in patients within the 6th day after the onset than those of sICAM-1 on the controls (P < 0.01). There was a positive correlation between both the levels of IL-6 and sICAM-1 at the first 3 days after the onset and the infarct volume (r = 0. 368, P < 0. 05 and r = 0. 594, P < 0. 01) , and the sICAM-1 positively correlated with IL-6 (r = 0. 453, P < 0. 05). CONCLUSION: The serum levels of IL-6 and sICAM-1 were upregulated, which might play a role in inflammatory lesion, and the upregulation of sICAM-1 may be related to the IL-6. The levels of IL-6 and sICAM-1 may reflect both the degree of pathologic lesion after the brain ischemia and the infarct volume.