RESUMO
Ganglioside mimicry by C.jejuni lipo-oligosaccharides (LOS) could induce the production of autoantibodies against gangliosides and the development of Guillain-Barré syndrome (GBS). The LOS biosynthesis region exhibits significant variation with different strains. Using PCR amplifications of genes from published LOS loci and sequencing the LOS biosynthesis loci, the eight GBS-associated C. jejuni strains from HeBei could be classified into four classes. The expression of sialylated LOS structures (class A) or non-sialylated LOS structures(class F, H and P) in the C. jejuni LOS is considered to be two different factors for the induction of GBS.
Assuntos
Campylobacter jejuni/genética , Genes Bacterianos , Loci Gênicos , Lipopolissacarídeos/genética , Oligossacarídeos/genética , Sequência de Bases , Campylobacter jejuni/isolamento & purificação , Campylobacter jejuni/patogenicidade , Síndrome de Guillain-Barré/microbiologia , Humanos , Lipopolissacarídeos/biossíntese , Dados de Sequência Molecular , Oligossacarídeos/biossínteseRESUMO
The knowledge about lead (Pb) sorption on soil-derived black carbons (SBCs) under different cultivation intensities of soils is limited. In this study, chemical and spectroscopic methods were applied to investigate the Pb sorption mechanisms on SBCs in soils from a forest land, a rubber plantation area, and a vegetable farm with none, less and highly intensive cultivation, respectively, that are located in the Hainan Island of China. Results showed that the specific surface area and cation exchange capacity of the SBCs from the less and highly intensive cultivation soils were 4.5- and 2.7-fold, and 1.3- and 1.8-fold higher compared to that of SBC from the no-cultivation soil, which subsequently enhanced the Pb sorption capacities of SBCs in iron exchange fraction. Ion exchange and hydrogen bonded Pb fractions together accounted for about 80% of total Pb sorbed on all SBCs at an externally added 1000 mg L-1 Pb solution concentration. The OC-O groups also played key roles in Pb sorption by forming complexes of OC-O-Pb-O and/or OC-O-Pb. Overall, SBCs in soils under all studied cultivation intensities showed high potential to sorb Pb (with the maximum absorbed Pb amount of 46.0-91.3 mg g-1), and increased Pb sorption capacities of the studied soils by 18.7-21.1 mg kg-1 in the stable fraction (complexation). Therefore, SBC might be a potential environment-friendly material to enhance the Pb immobilization capacity of soil.
Assuntos
Poluentes Ambientais/química , Chumbo/química , Solo/química , Fuligem/química , Adsorção , China , Poluentes Ambientais/isolamento & purificação , Ferro , Chumbo/isolamento & purificaçãoRESUMO
Caspase-12 has been localized to endoplasmic reticulum (ER) and showed to involve ER stress-induced apoptosis. In the present work we investigated the temporospatial alterations of caspase-12 immunoreactivity in the penumbra following cerebral ischemia/reperfusion in rabbit. Transient cerebral ischemia was produced by intraluminal occlusion of the middle cerebral artery for 2 h followed by 1 h, 6 h, 1 day, 3 days, 7 days and 14 days of reperfusion. Caspase-12 immunohistochemistry was first increased in the penumbra 1 h after reperfusion, with a peak at day 1 to day 3, and then gradually decreased to basal level at day 14. The number of TUNEL-positive cells and ultrastructural observation of brain sections in the penumbra showed a similar change at the same time points. ER mediated by caspase-12 participated in apoptosis induced by cerebral ischemia/reperfusion injury, which may provide a new area for therapeutic intervention to ameliorate outcomes following cerebral ischemia.
Assuntos
Apoptose/fisiologia , Caspase 12/metabolismo , Cérebro/enzimologia , Retículo Endoplasmático/enzimologia , Traumatismo por Reperfusão/enzimologia , Animais , Cérebro/patologia , Cérebro/ultraestrutura , Seguimentos , Imuno-Histoquímica , Infarto da Artéria Cerebral Média/complicações , Infarto da Artéria Cerebral Média/enzimologia , Infarto da Artéria Cerebral Média/patologia , Masculino , Coelhos , Traumatismo por Reperfusão/etiologia , Traumatismo por Reperfusão/patologia , Fatores de TempoRESUMO
BACKGROUND: Intracerebral hemorrhage (ICH) results in secondary brain edema and injury that may lead to death and disability. ICH also causes inflammation. It is unclear whether inflammation contributes to brain edema and neuron injury or functions in repairing the brain tissue. AIMS: To understand the effect of inflammation in ICH, we have carried out an investigation on the various aspects and the dynamic changes of inflammation. SETTINGS AND DESIGN: An ICH model was generated by injecting 50 microl autologous tail artery blood stereotactically into the right caudate nucleus of 30 rats, which were randomly divided into five ICH groups. Similarly, five Sham control groups were generated by inserting the needle to the right caudate nucleus of rats. MATERIALS AND METHODS: Rat behavior was evaluated over the time course (6 h, 24 h, 48 h, 72 h and 7 d) in each group. The rats were then killed by administering an overdose of pentobarbital. Following the euthanasia, the brain water content, neuronal loss, glia proliferation, inflammatory infiltration and brain morphology of the rats were measured. Additionally, the expression of TNF-alpha, IL-6, ICAM-1, VEGF, NF-kappaB, C3 and CR2 was analyzed by immunohistochemistry. STATISTICAL ANALYSIS: The data were analyzed by student's t test. RESULTS: Rat brain water content increased progressively over the time course and reached its peak at 48 h followed ICH. The maximum of inflammatory infiltrate (especially neutrophils) and immunopositive cells of TNF-alpha, IL-6 and NF-kappaB, were at 48 h. The expression of C3 and CR2 reached their peaks at 48-72 h, while the expression ICAM-1 and VEGF were at maximum at 72 h followed ICH. CONCLUSIONS: The results suggested that the inflammatory cytokines, complement system and VEGF may have a function in the development of the brain edema and neuron injury followed ICH.
Assuntos
Edema Encefálico/imunologia , Hemorragia Cerebral/imunologia , Mediadores da Inflamação/metabolismo , Animais , Edema Encefálico/etiologia , Edema Encefálico/patologia , Hemorragia Cerebral/complicações , Hemorragia Cerebral/patologia , Complemento C3/biossíntese , Inflamação , Molécula 1 de Adesão Intercelular/biossíntese , Interleucina-6/biossíntese , Masculino , Modelos Animais , NF-kappa B/biossíntese , Ratos , Ratos Sprague-Dawley , Receptores de Complemento 3d/biossíntese , Fator de Necrose Tumoral alfa/biossíntese , Fator A de Crescimento do Endotélio Vascular/biossínteseRESUMO
OBJECTIVE: To study the relationship between the susceptibility to two subtypes of Guillain-Barre syndrome(GBS) AIDP and AMAN and the frequency of HLA-class I and II alleles as well as to approach the characteristics of AIDP and AMAN patients in immune genetics. METHODS: A case control research was done on 31 AIDP and 33 AMAN and 132 health individuals. DNA was extracted from peripheral blood leucocytes by improved fast salting out. HLA genes were typed with DNA-based technology and PCR-sequence specific primers (PCR-SSP) method. RESULTS: HLA-A33 frequency of HLA-class I, and DR16 and DQ5 frequencies of HLA-class II showed a significant increase in AIDP group as compared with the control. Relative risk (RR) was 6.13, 8.28 and 3.47 respectively. Corrected probability (Pc) was 0.011, 0.014 and 0.025(P < 0.05). HLA-B15,B35 frequency of HLA-class I showed a significant increase in patients with AMAN as compared with the controls,RR was 4.09 and 7.08 respectively, Pc was 0.015 and 0.000 8 respectively. CONCLUSIONS: HLA-A33, DR15 and DQ5 may have association with susceptibility to AIDP; HLA-B15, B35 may have association with susceptibility to AMAN. HLA-class II genes were not found to have any association with AMAN.
Assuntos
Síndrome de Guillain-Barré/genética , Antígenos HLA-A/genética , Antígenos HLA-B/genética , Antígenos HLA-DP/genética , Antígenos HLA-DQ/genética , Antígenos HLA-DR/genética , Síndrome de Miller Fisher/genética , Adulto , Estudos de Casos e Controles , Feminino , Frequência do Gene , Síndrome de Guillain-Barré/imunologia , Antígenos HLA-A/classificação , Antígenos HLA-B/classificação , Antígenos HLA-DP/classificação , Antígenos HLA-DQ/classificação , Antígenos HLA-DR/classificação , Teste de Histocompatibilidade , Humanos , Masculino , Síndrome de Miller Fisher/imunologiaRESUMO
BACKGROUND: The monosialoganglioside (GM1) is a popular topic of research but the bibliometric analysis of GM1 over the decades in Science Citation Index-Expanded (SCI-E) remains poorly understood. OBJECTIVE: To identify the global research and to improve the understanding of research trends in the GM1 field from 1942 to 2011. DESIGN: A bibliometric study. DATA RETRIEVAL: We performed a bibliometric analysis based on the SCI-E published by the Institute of Scientific Information. INCLUSIVE CRITERIA: Articles closely related to GM1 were included. Exclusive criteria: (1) Articles related to gangliosidosis, disialo-ganglioside, trisialo-ganglioside or ganglioside GQIb. (2) Document types such as meeting abstracts, reviews, proceedings papers, notes, and letters. MAIN OUTCOME MEASURES: (1) Type of publication output; (2) number of author outputs; (3) distribution of output in subject categories; (4) publication distribution of countries; (5) distribution of output in journals, and (6) distribution of citations in each decade. RESULTS: During 1942 to 2011, there were 10 126 papers on GM1 that were added to the SCI. Articles (8 004) were the most frequently used document type comprising 79.0%, followed by meeting abstracts, reviews and proceedings papers. Research on GM1 could be found in the SCI from 1942, it was developed in the 1970s, greatly increased in the 1980s, and reached a peak in the 1990s, and it was slightly decreased in 2000. The distribution of subject categories showed that GM1 research covered both clinical and basic science research. The USA, Japan, and Germany were the three most productive countries, and the publication numbers in the USA were highest in all decades. The Journal of Biological Chemistry, Journal of Neurochemistry and Biochemistry were core subject journals in GM1 studies in each decade. CONCLUSION: This study highlights the topics in GM1 research that are being published around the world.
RESUMO
Administration of vascular endothelial growth factor (VEGF) has been shown to increase cerebral blood flow and reduce neurological damage after experimental ischemic brain injury. The purpose of this study was to examine the optimal dose and time window for the neuroprotective effect of VEGF when administrated after focal ischemia/reperfusion injury in rabbits. Focal cerebral ischemia/reperfusion was induced by the middle cerebral artery occlusion (MCAO) method. In a dose response experiment, low (1.25 ng/µL), middle (2.5 ng/µL) and high (5.0 ng/µL) doses of VEGF were administered 2h after MCAO by the route of perifocal region. The VEGF at a dose of middle (2.5 ng/µL) displayed excellent effects on neuroprotective efficacy for focal cerebral ischemia/reperfusion injury. In another experiment, 2.5 ng/µL VEGF was administered at times varying from 2 to 8h after MCAO. Infarct volume, water content and neurological deficits were significantly reduced when VEGF was given at 2 and 3h after injury. The protective effect was less when the same dose was given at the later times. Thus, the present findings indicated that VEGF reduced ischemic neuronal danger with a therapeutic time window within the first 3h of transient MCAO and may be useful in the treatment of acute ischemic stroke in humans.
Assuntos
Isquemia Encefálica/tratamento farmacológico , Fármacos Neuroprotetores/farmacologia , Traumatismo por Reperfusão/tratamento farmacológico , Fator A de Crescimento do Endotélio Vascular/farmacologia , Animais , Isquemia Encefálica/metabolismo , Isquemia Encefálica/patologia , Imagem de Difusão por Ressonância Magnética/métodos , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Masculino , Coelhos , Ratos , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/patologia , Fatores de Tempo , Fator A de Crescimento do Endotélio Vascular/administração & dosagemRESUMO
OBJECTIVE: Occluding the middle cerebral artery of small animals with an intraluminal filament to build a stroke model has gained increasing acceptance. In light of the growing demand for magnetic resonance imaging (MRI) studies using the clinical MRI scanner, large animal models can be superior to small animal models. In this work, we developed a modified rabbit model of stroke, which was assessed using clinical MRI scanner and compared with a most commonly silicone-coated filament model. METHODS: We presented a focal cerebral ischemia in rabbits. The key feature of this modified method is the use of a guide wire as a 'nylon suture'. At 3 days after ischemia, the percentage of brain infarct volume, neurobehavioral score, intracranial hemorrhagic incidence and dynamic changes of T(2) and apparent diffusion coefficient values were assessed respectively and compared between the focal cerebral models. RESULTS: Wire-induced models had more severe brain infarct size with less dispersion (32.7 +/- 6.5%, coefficient of variation=0.20) than that with filament models (25.4 +/- 8.9%, coefficient of variation=0.31; p<0.05). There were more significant MRI changes in the early stage, higher rate of technique success (wire, 20/20; filament, 17/20) and less intracranial hemorrhage (wire, 0/20; filament, 3/20) in wire-induced models than in filament-induced rabbits (p<0.05). CONCLUSION: Our data suggest that wire-induced method can provide a useful tool for the earlier research of ischemia.
Assuntos
Encéfalo/patologia , Infarto da Artéria Cerebral Média/patologia , Acidente Vascular Cerebral/patologia , Análise de Variância , Animais , Encéfalo/fisiopatologia , Modelos Animais de Doenças , Infarto da Artéria Cerebral Média/complicações , Infarto da Artéria Cerebral Média/fisiopatologia , Imageamento por Ressonância Magnética , Coelhos , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/fisiopatologiaRESUMO
The aim of this study was to establish an animal model of experimental allergic encephalomyelitis (EAE) and examine the basic pathological changes, as well as expression and distribution of MMP-2 and MMP-9, in Wistar rats. Tissue sections were processed for HE staining, Weil myelin staining, and modified Bielschowsky staining. Expression and distribution of glial fibrillary acidic protein (GFAP), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) were detected with immunohistochemistry. We divided the EAE into five types, depending on pathological characteristics and clinical manifestations: acute EAE, relapsing-remitting EAE, progressive EAE, benign EAE, and asymptomatic EAE. Rats with acute EAE suffered from quick, severe attacks with widespread inflammatory cells and axonal loss. No demyelination or astrocytic hyperplasia was found around the lesions. Rats with relapsing-remitting EAE broke down twice, with many perivascular cuffs and demyelinating plaques in lesions; hyperplastic and hypertrophic astrocytes characterized old lesions and axonal loss was evident. Rats suffering from progressive EAE exhibited continuous aggravation without improvement, accompanied by perivascular cuffs, demyelination, increased gliocytes and axonal damage. Rats with benign EAE recovered to a normal state with obviously decreased inflammatory cells and almost entirely unaffected myelin and axons. Rats with asymptomatic EAE also had various pathological changes that were not coincident with their clinical manifestations. Elevated expression of MMP-2 and MMP-9 was concordant in different types of EAE, but the extent differed in each type of EAE. MMP-2 and MMP-9 can be expressed in the form of vascular endothelial cells, meninges, or accumulated inflammatory cells. Multiple clinical courses of disease were demonstrated in Wistar rat EAE, with attributes similar to multiple sclerosis (MS) in clinical and pathological characteristics. Elevated expression of MMP-2 and MMP-9 may play a role in some aspects of pathological changes in EAE, for example, destroying the blood-brain barrier, degrading the myelin sheath, and damaging axons.
Assuntos
Modelos Animais de Doenças , Encefalomielite Autoimune Experimental/patologia , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Esclerose Múltipla/patologia , Animais , Astrócitos/patologia , Axônios/patologia , Encéfalo/enzimologia , Encéfalo/patologia , Encefalomielite Autoimune Experimental/enzimologia , Feminino , Proteína Glial Fibrilar Ácida/metabolismo , Imuno-Histoquímica , Esclerose Múltipla/enzimologia , Bainha de Mielina/patologia , Ratos , Ratos Wistar , Medula Espinal/enzimologia , Medula Espinal/patologia , Coloração e RotulagemRESUMO
OBJECTIVE: To search the marker proteins of Guillain-Barré syndrome (GBS)-associated Campylobacter jejuni (C. jejuni) by comparing the protein maps of GBS-associated C. jejuni strains with that of non-GBS-associated C. jejuni strains. METHODS: The whole-cell proteins of eight GBS-associated and eight non-GBS-associated C. jejuni strains were separated using the two-dimensional gel electrophoresis respectively. The differentially expressed proteins between the two sets of strains were identified by matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS) after in-gel tryptic digestion. RESULTS: Twenty differentially expressed spots were found with seventeen identified ones using MSCOT database. These proteins were identified as wlaX protein and some other proteins involving in energy metabolism (malate dehydrogenase, triosephosphate isomerase, Ni/Fe-hydrogenase small chain, cysteine synthase, branched-chain amino acid aminotransferase), cell process (heat shock protein, iron-uptake ABC transport system periplasmic iron-binding protein, alkyl hydroperoxide reductase), cell envelope (flagellin, UDP-N-acetylenolpyruvoylglucosamine reductase) etc. CONCLUSION: WlaX proteins were probably associated with LPS biosynthesis or virulence of C. jejuni. WlaX protein and flagellin protein were the possible marker-proteins of GBS-associated C. jejuni strains.