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BACKGROUND: Epimedin A (EA) has been shown to suppress extensive osteoclastogenesis and bone resorption, but the effects of EA remain incompletely understood. The aim of our study was to investigate the effects of EA on osteoclastogenesis and bone resorption to explore the corresponding signalling pathways. METHODS: Rats were randomly assigned to the sham operation or ovariectomy group, and alendronate was used for the positive control group. The therapeutic effect of EA on osteoporosis was systematically analysed by measuring bone mineral density and bone biomechanical properties. In vitro, RAW264.7 cells were treated with receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) to induce osteoclast differentiation. Cell viability assays, tartrate-resistant acid phosphatase (TRAP) staining, and immunofluorescence were used to elucidate the effects of EA on osteoclastogenesis. In addition, the expression of bone differentiation-related proteins or genes was evaluated using Western blot analysis or quantitative polymerase chain reaction (PCR), respectively. RESULTS: After 3 months of oral EA intervention, ovariectomized rats exhibited increased bone density, relative bone volume, trabecular thickness, and trabecular number, as well as reduced trabecular separation. EA dose-dependently normalized bone density and trabecular microarchitecture in the ovariectomized rats. Additionally, EA inhibited the expression of TRAP and NFATc1 in the ovariectomized rats. Moreover, the in vitro results indicated that EA inhibits osteoclast differentiation by suppressing the TRAF6/PI3K/AKT/NF-κB pathway. Further studies revealed that the effect on osteoclast differentiation, which was originally inhibited by EA, was reversed when the TRAF6 gene was overexpressed. CONCLUSIONS: The findings indicated that EA can negatively regulate osteoclastogenesis by inhibiting the TRAF6/PI3K/AKT/NF-κB axis and that ameliorating ovariectomy-induced osteoporosis in rats with EA may be a promising potential therapeutic strategy for the treatment of osteoporosis.
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Diferenciación Celular , FN-kappa B , Osteoclastos , Fosfatidilinositol 3-Quinasas , Proteínas Proto-Oncogénicas c-akt , Transducción de Señal , Factor 6 Asociado a Receptor de TNF , Animales , Factor 6 Asociado a Receptor de TNF/metabolismo , Factor 6 Asociado a Receptor de TNF/genética , Osteoclastos/metabolismo , FN-kappa B/metabolismo , Transducción de Señal/efectos de los fármacos , Diferenciación Celular/efectos de los fármacos , Proteínas Proto-Oncogénicas c-akt/metabolismo , Femenino , Fosfatidilinositol 3-Quinasas/metabolismo , Ratas , Ratones , Células RAW 264.7 , Flavonoides/farmacología , Osteogénesis/efectos de los fármacos , Ratas Sprague-Dawley , Osteoporosis/metabolismo , Osteoporosis/etiología , Ovariectomía/efectos adversos , Regulación de la Expresión Génica/efectos de los fármacos , Densidad Ósea/efectos de los fármacosRESUMEN
Pecan (Carya illinoinensis) is an important economic forest crops widely cultivated in China. From June to September in both 2021 and 2022, severe leaf disease resembling anthracnose was observed in 6.6-ha pecan orchard in Jintan (31°42'23.84â³ N, 119°21'22.90â³ E), Jiangsu Province. The disease severity was about 15 to 25% with 5 to 12% incidence on 100 surveyed trees of the orchard in 2022. Symptoms initially appeared as small gray-bark sunken lesions, which gradually developed to big sunken lesions with brown edges and irregular-shaped. Small fragments (4 × 4 mm) from the necrotic borders of infected leaves were surfaced sterilized, plated on potato dextrose agar (PDA) and then incubated in darkness at 25°C for 3 days. Pure cultures were obtained by monosporic isolation. Twenty-one isolates with similar characteristics were obtained from the infected leaves (isolation frequency about 90%). The upper side of colonies on the PDA plates was milky, and the reverse side was pale yellow at the center and pale white at the margin. After 10 days of growth on the PDA medium, these isolates produced spores separately. . Through electron microscopic observation, conidia were smooth walled, hyaline, aseptate, guttulate, cylindrical with rounded ends with 15 to 20.5 × 5.3 to 6.7 µm (mean 18.5 × 5.8 µm, n = 50) in size. These morphological characteristics were similar to those of the species of Colletotrichumspp (Weir et al. 2012, Fu et al. 2019). To further identify the isolates, the regions of internal transcribed spacer (ITS), actin (ACT), calmodulin (CAL), chitin synthase (CHSI), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and beta-tubulin 2 (TUB2) loci of the three representative isolates (JSJT-1, JSJT-2, and JSJT-3) were amplified and sequenced with the primer pairs ITS-1F/ITS-4, ACT-512F/ACT-783R, CL1/CL2A, CHS-79F/CHS-345R, GDF/GDR and T1/T2 primers, respectively (Weir et al. 2012). Sequences of them were deposited in GenBank under nos. OR214960 to OR214962 (ITS), OR228543 to OR228545 (ACT)ï¼OR228546 to OR228548 (CAL), OR228549 to OR228551 (CHSI), OR228552 to OR228554 (GAPDH), and OR228555 to OR228557 (TUB2). Multilocus phylogenetic analysis revealed that the three isolates and C. aenigma were clustered in the same clade. Based on the results of morphological and molecular analysis, these isolates were identified as C. aenigma. The pathogenicity of three isolates was tested on leaves of pecan seedlings. Suspensions of conidia were obtained by scraping the surface of a 10-day-old sporulated petri dish PDA cultures into sterile water. Suspensions were adjusted to a density of 2 × 106 conidia/ml with a hemocytometer.The conidial suspension of each isolate was sprayed evenly on the surface of leaves from three healthy pecan seedlings. Sterilized distilled water was used for negative controls. The pathogenicity experiment was repeated three times. Finally, all inoculated plants were kept in a light-incubator at 28°C under 100% relative humidity and 12 h photoperiod. Two weeks after inoculation, the inoculated plants developed symptoms similar to those of the original diseased plants, while controls remained asymptomatic. C. aenigma were re-isolated from from inoculated leaves. C. aenigma has been reported as the causal agent of anthracnose on several economically important plants, such as grape ( Kim et al. 2021), tree peonies (Wang et al.2023), chili (Diao et al. 2017), and pear (Fu et al. 2019), but this is the first report of C. aenigma causing anthracnose on pecan in China. Identification of C. aenigma as a pathogen of pecan is important for implementing control management strategies for pecan disease. References: Diao, Y. Z., et al. 2017. Persoonia. 38:20. Fu, M., et al. 2019. Persoonia. 42:1. Kim, J. S., et al. 2021. Plant Dis. 105:2729. Weir, B. S., et al. 2012. Stud. Mycol.. 73:115. Wang, Y. L., et al. 2023. Plant Dis. 107(4):1242. The author(s) declare no conflict of interest. Keywords: Colletotrichum aenigma, Anthracnose, Carya illinoinensis, Pathogenicity.
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Pecan (Carya illinoinensis) is one of the important economic forest crops widely cultivated in Jiangsu Provinces, China. From August to September in both 2021 and 2022, a foliar blight was observed in 7-ha and 6-ha pecan orchards in Changzhou (31°58'9.6â³ N, 119°48'33.84â³ E), and Jurong (31°52'15.46â³ N, 119°9'24.62â³ E), Jiangsu Province. The disease severity was about 32% with 8% incidence on 120 surveyed trees of the two orchards. Typical symptoms were lesions with a dark-brown color, which later became brown. We collected eighteen pecan leaves with typical symptoms in the surveyed pecan orchards and took them back to the laboratory for identification. Small fragments (approximately 9 mm2) from the necrotic borders of infected leaves were surfaced sterilized, plated on potato dextrose agar (PDA) and then incubated in darkness at 25°C. Pure cultures were obtained by single-spore culture. Thirty-three isolates with similar characteristics were obtained from the infected leaves (isolation frequency 85%), and the colonies surface on PDA was ochreous with patchs of olivaceous-yellow and sparse aerial mycelium. Observing from the back of the plate, the colonies were cream-yellow. Two types of single-cell conidia were produced on PDA. Alpha-conidia were 7.4 (range, 5.9 to 8.8) × 2.1 (range, 1.6 to 2.8) µm (n = 100), aseptate, smooth, fusiform, straight and tapering towards both ends. Beta-conidia were 25.1 (range, 19.1 to 36.2) × 1.3 (range, 1.0 to 2) µm (n = 100), filiform, hyaline, aseptate and curved at one end. The morphological features of these isolates agreed with those of Diaporthe sp. (Gomes et al. 2013; Gao et al. 2017). To further identify the isolates, the regions of internal transcribed spacer (ITS, OR214967 to OR214969), calmodulin (CAL, OR228558 to OR228560), translation elongation factor 1-α (EF1a, OR228561 to OR228563), histone H3 (HIS, OR228564 to OR228566), and beta-tubulin 2 (TUB2, OR228567 to OR228569) were amplified and sequenced from genomic DNA for the three representative isolates (LSM1, LSM2 and LSM3), respectively (Gomes et al. 2013). Multilocus phylogenetic analysis revealed that the three isolates and D. pseudophoenicicola were clustered in the same clade. Based on the results of morphological and molecular analysis, these isolates were identified as D. pseudophoenicicola. The pathogenicity of three isolates were tested on leaves of pecan seedlings. The conidial suspension (1 × 105 conidia/ml) of each isolate was sprayed evenly on the surface of leaves of three healthy seedlings. Sterilized distilled water was used for negative controls. Finally, all inoculated plants were kept in a greenhouse at 28°C under 100% relative humidity. Two weeks after inoculation, the inoculated plants developed symptoms similar to those of the original diseased plants, while controls remained asymptomatic. D. pseudophoenicicola were re-isolated from from inoculated plants. The pathogenicity experiment was repeated three times. Previously, D. pseudophoenicicola has been reported to cause stem-end browning disease in ripe mango (Takushi et al. 2016; Xu et al 2022). To our knowledge, this is the first report of D. pseudophoenicicola causing leaf blight on pecan . This study provides important information for developing effective pecan disease management practices.
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BACKGROUND: The study was aimed at finding accurate and effective therapeutic targets and deepening our understanding of the mechanisms of advanced atherosclerosis (AA). METHODS: We downloaded the gene expression datasets GSE28829, GSE120521, and GSE43292 from Gene Expression Omnibus. Weighted gene coexpression network analysis (WGCNA) was performed for GSE28829, and functional enrichment analysis and protein-protein interaction network analysis were conducted on the key module. Significant genes in the key module were analyzed by molecular complex detection, and genes in the most important subnetwork were defined as hub genes. Multiple dataset analyses for hub genes were conducted. Genes that overlapped between hub genes and differentially expressed genes (DEGs) of GSE28829 and GSE120521 were defined as key genes. Further validation for key genes was performed using GSE28829 and GSE43292. Gene set enrichment analysis (GSEA) was applied to key genes. RESULTS: A total of 77 significant genes in the key module of GSE28829 were screened out that were mainly associated with inflammation and immunity. The subnetwork was obtained from significant genes, and 18 genes in this module were defined as hub genes, which were related to immunity and expressed in multiple diseases, particularly systemic lupus erythematosus. Some hub genes were regulated by SPI1 and associated with the blood, spleen, and lung. After overlapping with DEGs of GSE28829 and GSE120521, a total of 10 genes (HCK, ITGAM, CTSS, TYROBP, LAPTM5, FCER1G, ITGB2, NCF2, AIF1, and CD86) were identified as key genes. All key genes were validated and evaluated successfully and were related to immune response pathways. CONCLUSION: Our study suggests that the key genes related to immune and inflammatory responses are involved in the development of AA. This may deepen our understanding of the mechanisms of and provide valuable therapeutic targets for AA.
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Aterosclerosis/genética , Aterosclerosis/inmunología , Aterosclerosis/patología , Bases de Datos Genéticas , Expresión Génica , Redes Reguladoras de Genes , Marcadores Genéticos , Humanos , Gravedad del Paciente , Mapas de Interacción de ProteínasRESUMEN
[This corrects the article DOI: 10.3389/fnins.2020.00215.].
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To fully exploit selenium-rich land resources and ensure crop safety, the phenomenon of "double high" of Se and heavy metals in reclaimed soil of mining wasteland was studied. Soil and maize samples collected from "point-to-point" were weighted by the inverse distance weighted (IDW) method; multiple linear regression (MLR), partial least squares regression (PLSR), random forest regression (RFR), and other methods were used to predict selenium uptake by maize in a sulfur mine reclamation area in southwest China. Meanwhile, the antagonistic effects of selenium (Se) on heavy metals (Hg, As, Cd, and Cr) were analyzed. The results showed that the soil in the study area was rich in selenium resources. The average Se content in the soil reached 0.83 mg·kg-1, which was 2.87 times that of the average Se content in Chinese soil. The Se content in maize grains ranged from 0.02 mg·kg-1 to 0.16 mg·kg-1. According to correlation analysis and model prediction, the main influencing factors of selenium content in maize grains in the study area were soil selenium, pH value, organic matter, and heavy metal As. Multivariate linear regression (MLR) was the most effective method for predicting selenium content in maize grains, and the determinant coefficient R2 was 0.52. By comparing the enrichment characteristics of maize to heavy metals (Hg, As, Cd, and Cr) under different concentration gradients of Se in the soil of the study area, the results showed that Se had antagonistic effects on Hg, As, Cd, and Cr. The results can provide a basis for the development of selenium-rich agriculture in similar mining wasteland reclamation in the future.
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Background: The mechanism of post-stroke cognitive impairment (PSCI) has not been explained. We aimed to investigate whether miR-let-7i participates in the PSCI and illuminates its underlying role in oxygen-glucose deprivation (OGD)-induced cell apoptosis. Methods: Blood samples from 36 subjects with PSCI and 38 with post-stroke cognitive normality (Non-PSCI) were collected to evaluate the differential expression of miR-let-7 family members, using qRT-PCT analysis. Spearman correlation was performed to estimate the correlation between the miR-1et-7i level and Montreal Cognitive Assessment (MoCA) score. Treatment of SH-SY5Y cells with OGD was used to induce cell apoptosis in vitro. Effects of miR-let-7i on OGD-induced cell apoptosis was estimated after transfection. The target gene of miR-let-7i was analyzed by dual luciferase reporter gene assay. Results: The expression of miR-let-7i was up-regulated in PSCI patients compared with Non-PSCI (p < 0.001) and negatively correlated with MoCA score (r = -0.643, p < 0.001). When exposed to OGD, SH-SY5Y cells showed significant apoptosis accompanied by miR-let-7i up-regulation. In OGD-treated cells, miR-let-7i up-regulation was accompanied by cell apoptosis, while down-regulation showed the opposite effect. Luciferase reporter assay showed that Bcl-2 was a target gene of miR-let-7i. Western blot showed that miR-let-7i up-regulation promoted Bcl-2 expression, while qRT-PCR showed that miR-let-7i had no effect on Bcl-2 expression. Conclusion: miR-let-7i was overexpressed in PSCI patients and it could be used as a diagnostic biomarker for PSCI. We illuminated the potential mechanism that miR-let-7i alleviated OGD-induced cell damage by targeting Bcl-2 at the post-transcriptional level.
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BACKGROUND: Neointimal hyperplasia, which is caused by dysfunction of vascular smooth muscle cells and vascular endothelial cells (VECs), is a foundation for later development of vein grafted occlusion. This study investigates whether neointimal hyperplasia could be prevented by the application of paeonol, a phenolic compound having functions of anti-inflammatory, anti-oxidant, and anti-proliferative. METHODS: Autologous jugular veins, which engrafted to carotid arteries in rabbits, were enveloped with paeonol or left untreated. After 0, 2, and 3 wk, vein grafts were respectively harvested. Proliferating cell nuclear antigen, vascular cell adhesion molecule l (VCAM-1), and intercellular cell adhesion molecule 1 were assessed with immunohistochemistry and Western blot. VECs apoptosis was also detected with terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling assay. RESULTS: Paeonol treatment reduced early neointimal hyperplasia by 42%-46% (P < 0.001) and early medial hyperplasia by 18%-22% (P < 0.001) compared with the controls. Immunohistochemical and Western blot results show a significant downregulation of proliferating cell nuclear antigen (P < 0.001) and VCAM-1 (P < 0.001) in paeonol treatment group in the second and third weeks. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling analysis discovered that VECs apoptosis was also reduced by the paeonol treatment in the second and third weeks (P < 0.001). CONCLUSIONS: Paeonol could prevent vein graft early restenosis by suppressing intimal and medial hyperplasia via inhibition of vascular smooth muscle cells proliferation, VCAM-1 expression, and anti-apoptosis of VECs in grafted veins.
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Acetofenonas/uso terapéutico , Antiinflamatorios/uso terapéutico , Arterias Carótidas/cirugía , Oclusión de Injerto Vascular/prevención & control , Venas Yugulares/trasplante , Neointima/prevención & control , Animales , Biomarcadores/metabolismo , Oclusión de Injerto Vascular/metabolismo , Oclusión de Injerto Vascular/patología , Hiperplasia/etiología , Hiperplasia/metabolismo , Hiperplasia/prevención & control , Venas Yugulares/metabolismo , Venas Yugulares/patología , Neointima/etiología , Neointima/metabolismo , Neointima/patología , Conejos , Distribución Aleatoria , Resultado del TratamientoRESUMEN
Aging has been attributed to oxidative stress and inflammatory response, in which NF-κB and Nrf2-ARE signaling pathways play significant roles. Senescence accelerated mouse prone 8 (SAMP8) is generally used an animal model for aging studies. Here, we investigated the NF-κB and Nrf2-ARE signaling pathways in SAMP8 brains at different ages and their responses to SS31 peptide treatment. Thirty six SAMP8 mice were separated into aging groups and SS31-treatment groups. The hippocampus from each mouse was dissected for RNA and protein extraction. Cytokines and ROS levels were measured using ELISA and standardised method. Gene expressions of NF-κB, Nrf2 and HO-1 were measured by RT-qPCR. Total protein amount of NF-κB and HO-1, as well as the concentrations of nuclear and cytoplasmic Nrf2 were measured using Western blots. Our data showed that aging could activate both NF-κB and Nrf2-ARE signaling pathways, which could be suppressed and activated by SS31 treatment respectively. Regression analysis revealed that NF-κB gene expression was the most important parameter predicting aging process and SS31 treatment effects in SAMP8. Our findings suggested that SS31 treatment may modulate the inflammatory and oxidative stress status of the aged brains and exert protective effects during brain aging.
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Envejecimiento/efectos de los fármacos , Envejecimiento/patología , Antioxidantes/farmacología , Disfunción Cognitiva/patología , FN-kappa B/genética , Oligopéptidos/farmacología , Envejecimiento/metabolismo , Envejecimiento/psicología , Animales , Disfunción Cognitiva/genética , Disfunción Cognitiva/metabolismo , Modelos Animales de Enfermedad , Masculino , Ratones , FN-kappa B/metabolismo , Estrés Oxidativo/efectos de los fármacos , Estrés Oxidativo/genética , Especies Reactivas de Oxígeno/metabolismo , Transducción de Señal/efectos de los fármacos , Transducción de Señal/genéticaRESUMEN
BACKGROUND: The detection of solitary pulmonary nodules (SPNs) that may potentially develop into a malignant lesion is essential for early clinical interventions. However, grading classification based on computed tomography (CT) imaging results remains a significant challenge. The 2-[18F]-fluoro-2-deoxy-D-glucose (18F-FDG) positron emission tomography (PET)/CT imaging produces both false-positive and false-negative findings for the diagnosis of SPNs. In this study, we compared 18F-FDG and 3-deoxy-3-[18F]-fluorothymidine (18F-FLT) in lung cancer PET/CT imaging. METHODS: The binding ratios of the two tracers to A549 lung cancer cells were calculated. The mouse lung cancer model was established (n = 12), and micro-PET/CT analysis using the two tracers was performed. Images using the two tracers were collected from 55 lung cancer patients with SPNs. The correlation among the cell-tracer binding ratios, standardized uptake values (SUVs), and Ki-67 proliferation marker expression were investigated. RESULTS: The cell-tracer binding ratio for the A549 cells using the 18F-FDG was greater than the ratio using 18F-FLT (P < 0.05). The Ki-67 expression showed a significant positive correlation with the 18F-FLT binding ratio (r = 0.824, P< 0.01). The tumor-to-nontumor uptake ratio of 18F-FDG imaging in xenografts was higher than that of 18F-FLT imaging. The diagnostic sensitivity, specificity, and the accuracy of 18F-FDG for lung cancer were 89%, 67%, and 73%, respectively. Moreover, the diagnostic sensitivity, specificity, and the accuracy of 18F-FLT for lung cancer were 71%, 79%, and 76%, respectively. There was an obvious positive correlation between the lung cancer Ki-67 expression and the mean maximum SUV of 18F-FDG and 18F-FLT (r = 0.658, P< 0.05 and r = 0.724, P< 0.01, respectively). CONCLUSIONS: The 18F-FDG uptake ratio is higher than that of 18F-FLT in A549 cells at the cellular level. 18F-FLT imaging might be superior for the quantitative diagnosis of lung tumor tissue and could distinguish lung cancer nodules from other SPNs.
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Fluorodesoxiglucosa F18/análisis , Neoplasias Pulmonares/diagnóstico por imagen , Tomografía Computarizada por Tomografía de Emisión de Positrones/métodos , Nódulo Pulmonar Solitario/diagnóstico por imagen , Células A549 , Animales , Humanos , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Tomografía Computarizada por Rayos XRESUMEN
Quantitative polymerase chain reaction (qPCR) was used to assess the abundance and relative distribution of host infection groups of the root-nodule forming, nitrogen-fixing actinomycete Frankia in four soils with similar physicochemical characteristics, two of which were vegetated with a host plant, Alnus glutinosa, and two with a non-host plant, Betula nigra. Analyses of DAPI-stained cells at three locations, i.e., at a distance of less than 1 m (near stem), 2.5 m (middle crown), and 3-5 m (crown edge) from the stems of both tree species revealed no statistically significant differences in abundance. Frankiae generally accounted for 0.01 to 0.04 % of these cells, with values between 4 and 36 × 10(5) cells (g soil)(-1). In three out of four soils, abundance of frankiae was significantly higher at locations "near stem" and/or "middle crown" compared to "crown edge," while numbers at these locations were not different in the fourth soil. Frankiae of the Alnus host infection group were dominant in all samples accounting for about 75 % and more of the cells, with no obvious differences with distance to stem. In three of the soils, all of these cells were represented by strain Ag45/Mut15. In the fourth soil that was vegetated with older A. glutinosa trees, about half of these cells belonged to a different subgroup represented by strain ArI3. In all soils, the remaining cells belonged to the Elaeagnus host infection group represented by strain EAN1pec. Casuarina-infective frankiae were not found. Abundance and relative distribution of Frankia host infection groups were similar in soils under the host plant A. glutinosa and the non-host plant B. nigra. Results did thus not reveal any specific effects of plant species on soil Frankia populations.
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Alnus/microbiología , Betula/microbiología , Frankia/crecimiento & desarrollo , Frankia/genética , Frankia/aislamiento & purificación , Raíces de Plantas/microbiología , Microbiología del Suelo , Árboles/crecimiento & desarrollo , Árboles/microbiologíaRESUMEN
Mitochondrial dysfunction, oxidative stress and ß -amyloid (Aß) formation are thought to cause neuronal and synaptic degeneration underlying cognitive decline in Alzheimer's disease (AD). The senescence-accelerated mouse-prone 8 (SAMP8) mice have been used as an animal model for mechanistic and translational research for AD. In the present study we characterized mitochondrial and synaptic alterations in SAMP8 mice relative to SAMR1control mice and explored a protective effect of the small molecule peptide SS31, a cell membrane penetrant antioxidant, on mitochondrial and synaptic protein integrity as well as cognitive performance. Electron microscopic analysis revealed mitochondrial/synaptic deterioration in 10 months-old SAMP8 relative to SAMR1 mice, with the changes in the former rescued following 8 weeks treatment with SS31 (5 mg/kg/day, i.p.). Elevation of Aß42, mitochondrial fission protein (DLP1, Fis1) and matrix protein cyclophilin D (CypD), and reductions of mitochondrial fusion protein (Mfn2) and synaptic (i.e., synaptophysin, postsynaptic density protein 95 and growth associated protein 43) proteins, were detected in hippocampal lysates in SAMP8 mice relative to SAMR1. The above altered protein expressions in the SAMP8 mouse brain were restored with the SS31 treatment. Moreover, the SS31 treatment rescued learning and memory deficits detected in 10 month-old SAMP8 mice. Together, the findings suggest that this mitochondria-targeting antioxidant peptide may be of potential utility for AD therapy, with its pharmacological efficacy involves lowering of central Aß levels and protection of mitochondrial homeostasis and synaptic integrity, which may help slow down cognitive decline.
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Envejecimiento/efectos de los fármacos , Péptidos beta-Amiloides/antagonistas & inhibidores , Trastornos del Conocimiento/tratamiento farmacológico , Mitocondrias/efectos de los fármacos , Oligopéptidos/uso terapéutico , Sinapsis/efectos de los fármacos , Envejecimiento/genética , Envejecimiento/patología , Animales , Antioxidantes/farmacología , Antioxidantes/uso terapéutico , Trastornos del Conocimiento/patología , Masculino , Ratones , Ratones Transgénicos , Mitocondrias/patología , Oligopéptidos/farmacología , Sinapsis/patologíaRESUMEN
BACKGROUND: Rheumatoid arthritis (RA) is a chronic, systemic autoimmune inflammatory disorder. Many methods have been used to observe the progress of RA. The purpose of this study was to observe the progress of RA in rats with 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT), magnetic resonance (MR) imaging and arthritis score, and analyze the relationships among different methods in evaluation of RA. METHODS: Sixteen healthy Sprague Dawley (SD) rats about 8-week old were randomly assigned to a RA group and a control group. Bovine type II emulsified incomplete Freud's adjuvant was used to induce arthritis in the RA group. Arthritis score of the rats in two groups were recorded, and (18)F-FDG PET/CT, MR imaging were performed both on the corresponding rats every 3 days. All the rats were sacrificed at week 5, and histopathological examination was performed on rat knees stained with haematoxylin and eosin. RESULTS: The arthritis score and the standard uptake value (SUV) of knee joints in RA rats increased with the progression of arthritis gradually. Both peaks of arthritis score and SUV appeared at 21 days after the first immune injection, then the arthritis score and SUV of knee joints decreased slowly. The arthritis scores of knee joints in RA rats were positively correlated with their SUV changes. The MR images were confirmed by the histopathological studies. CONCLUSION: PET/CT can detect the earliest molecular metabolism changes of RA, and MR imaging can follow up the dynamical anatomical changes of RA, all of which indicated that PET/CT and MR imaging may be applied as useful tools to monitor the progress of RA.
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Artritis Reumatoide/diagnóstico , Fluorodesoxiglucosa F18 , Radiofármacos , Animales , Artritis Reumatoide/patología , Imagen por Resonancia Magnética , Tomografía de Emisión de Positrones , Ratas , Ratas Sprague-Dawley , Tomografía Computarizada por Rayos XRESUMEN
BACKGROUND: Quantitative T2 mapping has been a widely used method for the evaluation of pathological cartilage properties, and the histological assessment system of osteoarthritis in the rabbit has been published recently. The aim of the study was to investigate the effectiveness of quantitative T2 mapping evaluation for articular cartilage lesions of a rabbit model of anterior cruciate ligament transection (ACLT) osteoarthritis. METHODS: Twenty New Zealand White (NZW) rabbits were divided into ACLT surgical group and sham operated group equally. The anterior cruciate ligaments of the rabbits in ACLT group were transected, while the joints were closed intactly in sham operated group. Magnetic resonance (MR) examinations were performed on 3.0T MR unit at week 0, week 6, and week 12. T2 values were computed on GE ADW4.3 workstation. All rabbits were killed at week 13, and left knees were stained with Haematoxylin and Eosin. Semiquantitative histological grading was obtained according to the osteoarthritis cartilage histopathology assessment system. Computerized image analysis was performed to quantitate the immunostained collagen type II. RESULTS: The average MR T2 value of whole left knee cartilage in ACLT surgical group ((29.05±12.01) ms) was significantly higher than that in sham operated group ((24.52±7.97) ms) (P=0.024) at week 6. The average T2 value increased to (32.18±12.79) ms in ACLT group at week 12, but remained near the baseline level ((27.66±8.08) ms) in the sham operated group (P=0.03). The cartilage lesion level of left knee in ACLT group was significantly increased at week 6 (P=0.005) and week 12 (P<0.001). T2 values had positive correlation with histological grading scores, but inverse correlation with optical densities (OD) of type II collagen. CONCLUSION: This study demonstrated the reliability and practicability of quantitative T2 mapping for the cartilage injury of rabbit ACLT osteoarthritis model.
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Ligamento Cruzado Anterior/fisiopatología , Cartílago Articular/fisiopatología , Osteoartritis/fisiopatología , Animales , Ligamento Cruzado Anterior/metabolismo , Cartílago Articular/metabolismo , Colágeno Tipo II/metabolismo , Imagen por Resonancia Magnética , Masculino , Osteoartritis/metabolismo , ConejosRESUMEN
OBJECTIVE: To observe the imaging findings of congenital megaureter in order to enhance the understanding of this disease. METHODS: Image data of 5 patients with congenital megaureter and 2 misdiagnosed patients were analyzed, and image findings of congenital megaureter were summarized.Elscint Prestig 2.0T superconductive magnetic resonance urography (MRU) with conventional sequence (spin-echo, T1WI560 ms/16 ms; fast spin-echo, T2WI 9600 ms/96 ms ) was performed. Raw data were acquired with fastspin-echo sequence from heavy T2-weighted image (9600 ms/120 ms). Post-processing method of MRU was the maximum intensity projection with three-dimensional reconstruction in the workstation. Intravenous pyelography (IVP) was conducted, in which X-rayfilms were taken 7 minutes, 15 minutes, and 30 minutes after injecting contrast agent, exceptthat in 2 patients the films were taken delayed at 60 and 90 minutes .X-ray retrograde pyelography was performed on 2 patients, successful in one butfailed in the other. RESULTS: The dilated ureter showed hypointensity on T1-weighted images and hyperintensity on T2-weighted images in conventional MRI. The mass wall was intact, uniform in thickness, and showing hypointensity on T1-weighted and T2-weighted images. The MRU images showed a retroperitoneal mass appearing as an elongated tubular cystic structure spreading from kidney to bladder. MRU also revealed dilated calices and renal pelvis, pelviureteric obstruction, and renal duplication. The main signs of congenital megaureter in X-urography was significant dilatation of ureter, or normal renal pelvis with ureter dilatation, hydronephrosis, deformity, and displacement. CONCLUSIONS: MRU with X-urography could visualizethe characteristics of congenital megaureter, including the dilation of renal pelvis and ureter, calculi, urinary tract duplication, and stenosis location. The two techniques can complement each other in disease diagnosis and provide more detailed information for preoperative treatment.
Asunto(s)
Imagen por Resonancia Magnética/métodos , Uréter/anomalías , Humanos , Uréter/patología , UrografíaRESUMEN
OBJECTIVE: To prepare magnetic resonance (MR) molecular probe for somatostain receptor expressed on breast cancer cell membranes and investigate its physico-chemical properties and imaging features in vitro. METHODS: Molecular probe was prepared through superparamagnetic iron oxide (SPIO) conjugated to somatostatin analog-octreotide (OCT) using chemical method. Its features at different Fe(2+) concentrations were tested by MTT assay and Prussian blue staining respectively. Molecular probes at different Fe(2+) concentration and various numbers of cells labeled with the probe at Fe(2+) concentrations of 20 mg/L were scanned with 1.5 Tesla MR. Resovist was used in control group when labeling cells. RESULTS: Various blue-staining particles were found in the cytoplasms of labeled cells with the molecular probes at different concentrations after Prussion blue staining and there were more particles with the increase of Fe(2+) concentration. The label rate of the probe was 96.15% which was higher than that in control group (80.00%). The bioactivity had no difference between labeled and non-labeled cells (P>0.05). There was remarkable low signal intensity on T(2)-weighed imaging and no evident artifacts for molecular probe when the concentration of Fe(2+) was 20 mg/L. The least number of labeled cells detected by MR in vitro was 6 x 10(6) when the concentration of Fe(2+) was 20 mg/L. CONCLUSION: Molecular probe, SPIO-OCT, can effectively label breast cells which express SSTR. The reasonable Fe(2+) concentration of labeled cells and imaging was 20 mg/L. There is a correlation between MR signal intensity in vitro and the number of labeled cells.