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1.
Oxid Med Cell Longev ; 2021: 2216314, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34616502

RESUMO

Objectives: Observational studies indicate that insomnia may increase risk of peptic ulcer disease (PUD). Our purpose is to clarify the possible causal relationship between insomnia and PUD by Mendelian randomization analyses. Methods: We carried out analyses using summary statistics data for genetic variants reported from a GWAS of insomnia (N = up to 1,331,010 individuals) and from a GWAS of PUD (N = up to 456,327 individuals). Three Mendelian randomization approaches were used to explore whether insomnia might play a causal role in PUD, and pathway and functional enrichment analyses were conducted to anticipate the underlying mechanisms. Results: Conventional Mendelian randomization analysis showed clear causality between insomnia and PUD; 1 SD increased insomnia incident was related to a 19% higher risk of PUD (P = 6.69 × 10-16; OR, 1.19 (95% CI, 1.14-1.24)). The associations between insomnia and PUD were consistent in the other two analyses performed using the weighted median method (P = 7.75 × 10-7; OR, 1.16 (95% CI, 1.09-1.23)) and MR-Egger regression (P = 5.00 × 10-3; OR, 1.27 (95% CI, 1.07-1.50)). Moreover, no evidence indicated a reverse causality between PUD events and insomnia symptoms. Pathway and functional enrichment analyses indicated that the mechanisms of insomnia effect on PUD may be through various ways, such as the immune system and oxidative stress. Conclusions: This Mendelian randomization study suggests insomnia as a causal risk factor for PUD. The potential mechanisms included may be immune and oxidative stress. These findings indicate that improving sleep quality could have substantial health benefits.

2.
J Physiol Biochem ; 2021 Oct 18.
Artigo em Inglês | MEDLINE | ID: mdl-34657993

RESUMO

As a highly evolutionarily conserved process, autophagy can be found in all types of eukaryotic cells. Such a constitutive process maintains cellular homeostasis in a wide variety of cell types through the encapsulation of damaged proteins or organelles into double-membrane vesicles. Autophagy not only simply eliminates materials but also serves as a dynamic recycling system that produces new building blocks and energy for cellular renovation and homeostasis. Previous studies have primarily recognized the role of autophagy in the degradation of dysfunctional proteins and unwanted organelles. However, there are findings of autophagy in physiological and pathological processes. In hepatocytes, autophagy is not only essential for homeostatic functions but also implicated in some diseases, such as viral hepatitis, alcoholic hepatitis, and hepatic failure. In the present review, we summarized the molecular mechanisms of autophagy and its role in several liver diseases and put forward several new strategies for the treatment of liver disease.

3.
Front Immunol ; 12: 695491, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34489943

RESUMO

Patients with liver disease are susceptible to infection with Vibrio vulnificus (V. vulnificus), but the specific reasons remain elusive. Through RNA-seq, we found that when mice with alcoholic liver disease (ALD) were infected with V. vulnificus by gavage, compared with the Pair group, the small intestinal genes affecting intestinal permeability were upregulated; and the number of differentially expressed genes related to immune functions (e.g., such as cell chemotaxis, leukocyte differentiation, and neutrophil degranulation) decreased in the liver, spleen, and blood. Further analysis showed that the number of white blood cells decreased in the Pair group, whereas those in the ALD mice did not change significantly. Interestingly, the blood bacterial load in the ALD mice was about 100 times higher than that of the Pair group. After the ALD mice were infected with V. vulnificus, the concentrations of T cell proliferation-promoting cytokines (IL-2, IL-23) decreased. Therefore, unlike the Pair group, ALD mice had weaker immune responses, lower T cell proliferation-promoting cytokines, and higher bacterial loads post-infection, possibly increasing their susceptibility to V. vulnificus infection. These new findings we presented here may help to advance the current understanding of the reasons why patients with liver disease are susceptible to V. vulnificus infection and provides potential targets for further investigation in the context of treatment options for V. vulnificus sepsis in liver disease patient.

4.
Emerg Microbes Infect ; 10(1): 1683-1690, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34348599

RESUMO

At the end of 2019, A new type of beta-CoV, SARS-CoV-2 emerged and triggered the COVID-19 pandemic, which spread overwhelmingly around the world in less than a year. However, the origin and direct ancestral viruses of SARS-CoV-2 remain unknown. RaTG13, a novel coronavirus found in bats in China's Yunnan Province, is the closest relative virus of the SARS-CoV-2 identified so far. In this study, a new SARS-CoV-2 related virus, provisionally named PrC31, was discovered in Yunnan province by retrospectively analyse bat next generation sequencing (NGS) data of intestinal samples collected in 2018. PrC31 shared 90.7% and 92.0% nucleotide identities to the genomes of SARS-CoV-2 and the bat SARSr-CoV ZC45, respectively. Sequence alignment of PrC31 showed that several genomic regions, especially orf1a and orf8 had the highest homology with those corresponding genomic regions of SARS-CoV-2 than any other related viruses. Phylogenetic analysis indicated that PrC31 shared a common ancestor with SARS-CoV-2 in evolutionary history. The differences between the PrC31 and SARS-CoV-2 genomes were mainly manifested in the spike genes. The amino acid homology between the receptor binding domains of PrC31 and SARS-CoV-2 was only 64.2%. Importantly, recombination analysis revealed that PrC31 underwent multiple complex recombination events (including three recombination breakpoints) involving the SARS-CoV and SARS-CoV-2 sub-lineages, indicating that PrC31 evolved from yet-to-be-identified intermediate recombination strains. Combined with previous studies, it is revealed that the beta-CoVs may possess a more complex recombination mechanism than we thought.


Assuntos
Quirópteros/virologia , Recombinação Genética , SARS-CoV-2/genética , SARS-CoV-2/isolamento & purificação , Sequência de Aminoácidos , Animais , China , Genoma Viral , Filogenia , SARS-CoV-2/classificação , Alinhamento de Sequência , Proteínas Virais/genética
6.
Environ Toxicol ; 36(9): 1742-1757, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34032369

RESUMO

Oxidative stress has been considered as an important cause of neurocyte damage induced by carbon monoxide (CO) poisoning; however, the precise mechanisms are not fully understood. The study aimed to elucidate the molecular mechanism and the neuroprotective effect of targeted regulatory nuclear factor erythroid2-related factor 2 (Nrf2) gene on acute brain injury in CO poisoning rats. An acute CO poisoning rat model was established by CO inhalation in hyperbaric oxygen chamber and followed by the administration of Nrf2 gene-loaded lentivirus. Mitochondrial membrane potential (ΔΨM), the levels of Nrf2, glutamate-cysteine ligase catalytic subunit (GCLC), catalase (CAT) and glutathione peroxidase (GSH-Px), and cell apoptosis were determined in brain tissue in rats. We found that CO poisoning could decrease ΔΨm of cells, slightly increase the expressions of Nrf2 and GCLC at mRNA and protein levels, reduce CAT and GSH-Px, and thus initiate apoptosis process. The Nrf2 gene treatment could obviously enhance the expressions of Nrf2 at mRNA and protein levels, and increase the concentrations of CAT and GSH-Px, maintain the ΔΨm of cells in brain tissue, significantly inhibit cell apoptosis as compared with the CO poisoning group (p < .05). These findings suggest that CO poisoning could induce oxidative stress and impair mitochondrial function of cells in brain tissue. The administration of Nrf2 gene could notably strengthen the antioxidant capacity of cells through regulating the downstream genes of Nrf2/antioxidant responsive element signal pathway, and positively protect cells against brain injury induced by acute severe CO poisoning.


Assuntos
Lesões Encefálicas , Intoxicação por Monóxido de Carbono , Fator 2 Relacionado a NF-E2 , Fármacos Neuroprotetores , Animais , Lesões Encefálicas/induzido quimicamente , Lesões Encefálicas/genética , Intoxicação por Monóxido de Carbono/genética , Fator 2 Relacionado a NF-E2/genética , Fator 2 Relacionado a NF-E2/metabolismo , Fármacos Neuroprotetores/farmacologia , Estresse Oxidativo , Ratos
7.
J Ophthalmol ; 2021: 6287083, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33532092

RESUMO

[This corrects the article DOI: 10.1155/2020/9537360.].

8.
Cell Death Dis ; 12(1): 111, 2021 01 21.
Artigo em Inglês | MEDLINE | ID: mdl-33479191

RESUMO

Hepatectomy is an effective therapeutic strategy for many benign and malignant liver diseases, while the complexity of liver anatomy and the difficulty of operation lead to complications after hepatectomy. Among them, post-hepatectomy liver failure (PHLF) is the main factor threatening the life of patients. At present, liver transplantation is an effective approach for PHLF. However, the application of liver transplantation has been largely limited due to the shortage of donors and the high cost of such operation. Therefore, it is urgently necessary to develop a new treatment for PHLF. Mesenchymal stem cells (MSCs) have become a new treatment regimen for liver diseases because of their easy access and low immunogenicity. Our study found that there were some subtle connections between MSCs and liver lipid metabolism in the PHLF model. We used MSC transplantation to treat PHLF induced by 90% hepatectomy. MSC transplantation could restore the mitochondrial function, promote the ß-oxidation of fatty acid (FA), and reduce the lipid accumulation of hepatocytes. In addition, interleukin 10 (IL-10), a cytokine with immunoregulatory function, had an important role in lipid metabolism. We also found that MSCs transplantation activated the mammalian target of rapamycin (mTOR) pathway. Therefore, we explored the relationship between mitochondrial damage and lipid metabolism abnormality or PHLF. MSCs improved mitochondrial function and corrected abnormal lipid metabolism by affecting the mTOR pathway in the treatment of PHLF. Collectively, MSC transplantation could be used as a potential treatment for PHLF.


Assuntos
Hepatectomia/métodos , Hepatócitos/metabolismo , Metabolismo dos Lipídeos/fisiologia , Falência Hepática/fisiopatologia , Falência Hepática/terapia , Células-Tronco Mesenquimais/metabolismo , Animais , Feminino , Humanos , Masculino , Ratos , Ratos Sprague-Dawley
9.
Front Physiol ; 11: 177, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32218743

RESUMO

Aim: The pathogenesis of non-alcoholic fatty liver disease is currently unclear, however, lipid accumulation leading to endoplasmic reticulum stress appears to be pivotal in the process. At present, FOXO1 is known to be involved in NAFLD progression. The relationship between necroptosis and non-alcoholic steatohepatitis has been of great research interest more recently. However, whether FOXO1 regulates ER stress and necroptosis in mice fed with a high fat diet is not clear. Therefore, in this study we analyzed the relationship between non-alcoholic steatohepatitis, ER stress, and necroptosis. Main Methods: Male C57BL/6J mice were fed with an HFD for 14 weeks to induce non-alcoholic steatohepatitis. ER stress and activation of necroptosis in AML12 cells were evaluated after inhibition of FOXO1 in AML12 cells. In addition, mice were fed with AS1842856 for 14 weeks. Liver function and lipid accumulation were measured, and further, ER stress and necroptosis were evaluated by Western Blot and Transmission Electron Microscopy. Key Findings: Mice fed with a high fat diet showed high levels of FOXO1, accompanying activation of endoplasmic reticulum stress and necroptosis. Further, sustained PA stimulation caused ER stress and necroptosis in AML12 cells. At the same time, protein levels of FOXO1 increased significantly. Inhibition of FOXO1 with AS1842856 alleviated ER stress and necroptosis. Additionally, treatment of mice with a FOXO1 inhibitor ameliorated liver function after they were fed with a high fat diet, displaying better liver condition and lighter necroptosis. Significance: Inhibition of FOXO1 attenuates ER stress and necroptosis in a mouse model of non-alcoholic steatohepatitis.

10.
Front Physiol ; 10: 412, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31024348

RESUMO

Background: The mortality rate of post-hepatectomy liver failure (PHLF) remains very high, and liver transplantation is the only effective treatment regimen for PHLF. Cell transplantation is a potential treatment for liver diseases. Previous studies have proved that mesenchymal stem cells (MSCs) have immunomodulatory functions. In the present study, we found that MSCs promoted glycogen synthesis and liver regeneration in the treatment of PHLF. MSC transplantation also improved the survival rate of rats after 90% partial hepatectomy (PH). In our current study, we aimed to determine the efficacy and mechanism of MSC transplantation in the treatment of PHLF. Methods: Mesenchymal stem cells were isolated from Sprague-Dawley rats and cultured using a standardized protocol. The MSCs were transplanted to treat acute liver failure induced by 90% PH. The therapeutic efficacy of MSCs on PHLF was verified through measuring alanine transaminase (ALT), aspartate aminotransferase (AST), international normalized ratio (INR), serum ammonia, liver weight to body weight ratio, blood glucose, and histology. To further study the mechanism of MSC transplantation in treatment for PHLF, we assessed the changes in the AKT/glycogen synthase kinase-3ß (GSK-3ß)/ß-catenin pathway. A-674563 (AKT inhibitor) and SB216763 (GSK-3ß inhibitor) were employed to validate our findings. SPSS version 19.0 was used for statistical analysis, and the independent-samples t-test was carried out to analyze the collected data. Results: Mesenchymal stem cell transplantation attenuated the liver injury in acute liver failure induced by 90% PH. MSC transplantation improved the glucose metabolism and survival rate in the PHLF model. The effect of MSC transplantation on hepatocyte proliferation might be related to AKT/GSK-3ß/ß-catenin pathway. Conclusion: Mesenchymal stem cell transplantation could be use as a potential treatment for PHLF.

11.
Biochem Biophys Res Commun ; 508(3): 682-689, 2019 01 15.
Artigo em Inglês | MEDLINE | ID: mdl-30528392

RESUMO

In recent years, transplantation of mesenchymal stem cells (MSCs) has attracted much attention as a potential cell-based therapy for acute liver failure (ALF). As an inducible enzyme, heme oxygenase 1 (HO-1) has been reported to have cytoprotective, anti-apoptotic and immunoregulatory effects. Autophagy, a conserved catabolic process in cells, may be an important pathway for MSCs to treat ALF. In this study, we aimed to explore whether MSCs treat ALF by regulating autophagy and whether HO-1 was involved in the same pathway. Bone marrow-derived MSCs were isolated from Sprague-Dawley rats and cultured according to an established protocol. Co-culture systems of MSCs and hepatocytes were used to assess autophagy in the treatment of ALF. Meanwhile, MSCs were transplanted into rats with d-galactosamine (Gal)-induced ALF. Autophagy inhibitor (3-methyladenine, 3-MA), HO-1 inhibitor (zinc protoporphyrin, ZnPP) and PI3K specific inhibitor (LY294002) were employed in the study. Blood samples and liver tissues were collected before euthanasia. Survival rate, liver function, inflammatory factors, histology, Ki67 and TUNEL staining were determined. MSCs transplantation alleviated ALF both in vivo and in vitro. Autophagy and autophagy-related proteins were significantly up-regulated during MSCs treatment. 3-MA attenuated the therapeutic effect of MSCs. Administration of LY294002 before ALF induction inhibited hepatocyte autophagy. During the MSCs treatment, the HO-1 expression was increased, while inhibiting HO-1 attenuated the therapeutic effect of MSCs as well as hepatocyte autophagy. These findings suggested MSCs could alleviate ALF by increasing the HO-1 expression, which played an important role in activating autophagy through PI3K/AKT signaling pathway.


Assuntos
Autofagia , Heme Oxigenase-1/metabolismo , Falência Hepática Aguda/enzimologia , Falência Hepática Aguda/terapia , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais/metabolismo , Animais , Autofagossomos/metabolismo , Autofagossomos/ultraestrutura , Hepatócitos/patologia , Hepatócitos/ultraestrutura , Inflamação/patologia , Fígado/lesões , Fígado/patologia , Falência Hepática Aguda/patologia , Masculino , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos Sprague-Dawley , Transdução de Sinais , Regulação para Cima
12.
J Alzheimers Dis ; 65(4): 1353-1364, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30124448

RESUMO

BACKGROUND: Weighted co-expression network analysis (WGCNA) is a powerful systems biology method to describe the correlation of gene expression based on the microarray database, which can be used to facilitate the discovery of therapeutic targets or candidate biomarkers in diseases. OBJECTIVE: To explore the key genes in the development of Alzheimer's disease (AD) by using WGCNA. METHODS: The whole gene expression data GSE1297 from AD and control human hippocampus was obtained from the GEO database in NCBI. Co-expressed genes were clustered into different modules. Modules of interest were identified through calculating the correlation coefficient between the module and phenotypic traits. GO and pathway enrichment analyses were conducted, and the central players (key hub genes) within the modules of interest were identified through network analysis. The expression of the identified key genes was confirmed in AD transgenic mice through using qRT-PCR. RESULTS: Two modules were found to be associated with AD clinical severity, which functioning mainly in mineral absorption, NF-κB signaling, and cGMP-PKG signaling pathways. Through analysis of the two modules, we found that metallothionein (MT), Notch2, MSX1, ADD3, and RAB31 were highly correlated with AD phenotype. Increase in expression of these genes was confirmed in aged AD transgenic mice. CONCLUSION: WGCNA analysis can be used to analyze and predict the key genes in AD. MT1, MT2, MSX1, NOTCH2, ADD3, and RAB31 are identified to be the most relevant genes, which may be potential targets for AD therapy.


Assuntos
Doença de Alzheimer/genética , Redes Reguladoras de Genes , Predisposição Genética para Doença/genética , Proteínas de Ligação a Calmodulina/genética , Feminino , Perfilação da Expressão Gênica , Humanos , Fator de Transcrição MSX1/genética , Masculino , Entrevista Psiquiátrica Padronizada , Metalotioneína/genética , RNA Mensageiro/metabolismo , Receptor Notch2/genética , Biologia de Sistemas , Proteínas rab de Ligação ao GTP/genética
13.
Biomed Res Int ; 2018: 1287127, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-31205932

RESUMO

The liver is the main metabolic organ in the body especially in lipometabolism and glycometabolism. Carbohydrates and fats disorders can result in insulin resistance in the liver. Metabolic imbalance can even lead to life-threatening conditions. Therefore, it is essential to maintain the normal metabolic function of the liver. When the liver is in a pathological state, liver metabolism homeostasis is damaged, and metabolic disorders will further aggravate liver disease. Consequently, it is essential to determine the relationship between liver diseases and metabolic disorders. Here we review a lot of evidence that liver diseases are closely related to lipometabolism and glycometabolism. Although the disorder of the liver metabolism is caused by different liver diseases, the break of metabolic balance is determined by changes in the state of the liver. We discuss the relationship between liver disease and metabolic changes, outline the process of how metabolic changes are regulated by liver diseases, and describe the role which metabolic changes play in the process and prognosis of liver disease.


Assuntos
Metabolismo dos Carboidratos , Metabolismo dos Lipídeos , Hepatopatias/metabolismo , Fígado/metabolismo , Animais , Humanos , Fígado/patologia , Hepatopatias/patologia
14.
Sci Rep ; 4: 7588, 2014 Dec 23.
Artigo em Inglês | MEDLINE | ID: mdl-25533850

RESUMO

While H2N2 viruses have been sporadically isolated from wild and domestic birds, H2N2 viruses have not been detected among human populations since 1968. Should H2N2 viruses adapt to domestic poultry they may pose a risk of infection to people, as most anyone born after 1968 would likely be susceptible to their infection. We report the isolation of a novel influenza A virus (H2N2) cultured in 2013 from a healthy domestic duck at a live poultry market in Wuxi City, China. Sequence data revealed that the novel H2N2 virus was similar to Eurasian avian lineage avian influenza viruses, the virus had been circulating for ≥ two years among poultry, had an increase in α2,6 binding affinity, and was not highly pathogenic. Approximately 9% of 100 healthy chickens sampled from the same area had elevated antibodies against the H2 antigen. Fortunately, there was sparse serological evidence that the virus was infecting poultry workers or had adapted to infect other mammals. These findings suggest that a novel H2N2 virus has been circulating among domestic poultry in Wuxi City, China and has some has increased human receptor affinity. It seems wise to conduct better surveillance for novel influenza viruses at Chinese live bird markets.


Assuntos
Patos/virologia , Vírus da Influenza A Subtipo H2N2 , Influenza Aviária , Doenças das Aves Domésticas , Animais , Anticorpos Antivirais/sangue , Anticorpos Antivirais/imunologia , China , Patos/sangue , Patos/imunologia , Humanos , Vírus da Influenza A Subtipo H2N2/genética , Vírus da Influenza A Subtipo H2N2/imunologia , Vírus da Influenza A Subtipo H2N2/isolamento & purificação , Influenza Aviária/sangue , Influenza Aviária/imunologia , Influenza Aviária/virologia , Doenças das Aves Domésticas/sangue , Doenças das Aves Domésticas/imunologia , Doenças das Aves Domésticas/virologia
15.
Zhonghua Liu Xing Bing Xue Za Zhi ; 34(5): 428-32, 2013 May.
Artigo em Chinês | MEDLINE | ID: mdl-24016428

RESUMO

OBJECTIVE: To understand the epidemiologic characteristics of dengue fever, imported from Myanmar to the border of Yunnan province, China. Viral molecular epidemiologic features were also studied. METHODS: Questionnaires were used on each diagnosed, suspected dengue fever, case or unknown cases with fever when coming from Myanmar entering the port and hospitals in Ruili city of Yunnan province. Serum samples of these patients were collected to detect IgM antibody against dengue virus and RT-PCR assay. Homology and phylogenetic tree based on the whole nucleotide sequence of PrM-C and NS5 gene of dengue virus were further analyzed. RESULTS: A total of 103 sera were collected from patients at acute stage in Ruili city in July to November 2008. Among them, 49 cases were confirmed for dengue fever according to IgM and nucleic acid testings. Except one, other 48 cases were all imported into Ruili, from Myanmar. Of those, 18 patients were residents from Mujie city of Myanmar and hospitalized in Ruili and the rest 30 patients were Chinese citizens who had finished business and returned from Myanmar. Two isolates of serum samples from the imported cases were identified and both homology and phylogenetic analysis were performed, using the nucleotide sequences of PrM and NS5 genes. They were divided into dengue type 1 (RLB61) and dengue type 3 (RLC31) and were closer to the dengue virus strains isolated from Southeast Asia countries. CONCLUSION: It is confirmed that an epidemic of dengue fever which was imported from Myanmar to Ruili city of Yunnan province, China. Evidence also showed that both type I and III epidemic strains of dengue virus did exist in Mujie city of Myanmar in 2008.


Assuntos
Vírus da Dengue/genética , Dengue/epidemiologia , Adolescente , Adulto , Criança , Pré-Escolar , China/epidemiologia , Feminino , Genótipo , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Epidemiologia Molecular , Mianmar/epidemiologia , Filogenia , RNA Viral/genética
16.
Acta Crystallogr Sect E Struct Rep Online ; 69(Pt 1): m19, 2013 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-23476320

RESUMO

In the binuclear copper(II) title complex, [Cu2(C9H7O4)4(C2H3N)2], an inversion centre is situtated at the mid-point of the Cu-Cu bond. The Cu(II) atom together with its four coordinated O atoms are in a distorted planar square arrangement while the nitro-gen and the other Cu(II) atom are located in apical positions. The whole mol-ecule looks like a paddle-wheel. In the crystal, chains are assembled along the b axis through C-H⋯O hydrogen bonds and slipped π-π inter-actions between the benzene rings of neighbouring mol-ecules [centroid-centroid distance = 3.6929 (3) Šand slippage = 0.641 (1) Å].

17.
Artigo em Chinês | MEDLINE | ID: mdl-22804985

RESUMO

OBJECTIVE: To study the sympathetic skin response (SSR) to the effects of N-hexane on autonomic nerves function in patients with chronic N-hexane poisoning. METHODS: The subjects in present study included 30 controls and 37 cases with chronic N-hexane poisoning. Also 37 patients were divided into 3 subgroups (mild, moderate and severe poisoning) according to diagnostic criteria of occupational diseases. All subjects were examined by SSR test and nerve conduction velocity (NCV) test. All patients were reexamined by SSR and NCV every 1 ∼ 2 months. The differences in SSR parameters (latency, amplitude) among groups were observed. In the severe poisoning subgroup, the changes of SSR and NCV parameters (conduction velocity, amplitude) in different poisoning stages were observed. RESULTS: There were significant differences in SSR latency of upper extremity among groups and the significant differences in SSR amplitude of upper and lower extremity among groups (P < 0.05). No significant differences in SSR parameters were found between the adjacent groups (P > 0.05). There were significant differences in SSR latency of upper extremity during different periods and the significant differences in SSR amplitude of upper and lower extremity during different periods among all groups (P < 0.05). The change of SSR parameters consistent with that in NCV. The longest SSR latency of upper extremity and the smallest SSR amplitudes of upper and lower extremity appears 1 - 2 months earlier than that of the smallest action potential amplitude. CONCLUSION: The damage of autonomic nerves induced by N-hexane increased with poisoning progresses. The damage of autonomic nerves corresponded with the damage of myelin sheath of large myelinated nerves, but which appeared 1 - 2 months earlier than the damage of axon of large myelinated nerves. SSR test may serve as a method to detect the damage of autonomic nerves function in patients with chronic N-hexane poisoning.


Assuntos
Hexanos/envenenamento , Condução Nervosa , Doenças Profissionais/fisiopatologia , Sistema Nervoso Simpático/fisiopatologia , Adolescente , Adulto , Vias Autônomas/fisiopatologia , Estudos de Casos e Controles , Feminino , Resposta Galvânica da Pele , Humanos , Masculino , Pele/inervação , Pele/fisiopatologia , Adulto Jovem
18.
J Food Prot ; 75(1): 112-7, 2012 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-22221362

RESUMO

In the present study, we developed a convenient, rapid, and sensitive immunochromatographic (IC) test strip to detect abrin in assay buffer and spiked abrin in test food samples. The abrin IC test strip was based on a sandwich format consisting of a monoclonal antibody and a polyclonal antibody. The anti-abrin A chain monoclonal antibody from mice was immobilized on a porous nitrocellulose membrane as a capture antibody, while the anti-abrin polyclonal antibody from rabbits was conjugated to colloidal gold particles, serving as a detection antibody. Both visual observation and quantitative analysis indicated that the lower detection of the strip was about 3 ng/ml when abrin was directly spiked into milk, orange juice, and drinking water at a concentration of 3 to 60 ng/ml; the analytical recovery rate was 92.2 to 128%. With this method, abrin spiked into food could be detected in less than 10 min. Moreover, the IC test strip showed no cross-reaction with the closely related phytotoxin ricin. Therefore, our test strip is an ideal candidate for the development of a kit for rapid and quantitative detection of abrin in food samples.


Assuntos
Abrina/análise , Cromatografia de Afinidade/métodos , Contaminação de Alimentos/análise , Abrina/imunologia , Animais , Anticorpos Monoclonais/imunologia , Coloide de Ouro/química , Humanos , Camundongos , Coelhos , Kit de Reagentes para Diagnóstico , Fitas Reagentes , Sensibilidade e Especificidade
19.
Hum Vaccin ; 7(8): 838-44, 2011 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-21817853

RESUMO

We used site-directed mutagenesis to mutate two key amino acid residues, Glu164 and Arg167, of abrin A chain (ABRA), creating a mutant ABRA(E164AR167L). The mutant ABRA(mABRA) encoded by mABRA(E164AR167L) was expressed in the cytoplasm of Escherichia coli, and used to develop an effective vaccine to protect mice against native abrin intoxication. The cytotoxicity of mABRA was dramatically reduced as compared to that of recombinant ABRA(rABRA) and native abrin, but the antigenicity and immunogenicity remained the same. Balb/c mice were vaccinated with purified mABRA, and survival was evaluated after challenge with native abrin. Mice that were given three vaccinations developed a protective immune response that was 100% protective against an intraperitoneal (i.p.) administration of 10×LD50 of native abrin. Furthermore, the sera from immunized mice provided complete passive protection for naive mice. This study describes the generation of a substantial amount of mABRA from E. coli and the potential application of mABRA as an effective vaccine candidate for humans, to protect against a high-dose of native abrin.


Assuntos
Abrina , Proteínas Recombinantes , Vacinas Sintéticas/imunologia , Abrina/biossíntese , Abrina/genética , Abrina/imunologia , Abrus/efeitos adversos , Animais , Anticorpos/sangue , Sequência de Bases , Escherichia coli/genética , Feminino , Camundongos , Camundongos Endogâmicos BALB C , Dados de Sequência Molecular , Mutagênese Sítio-Dirigida , Mutação , Proteínas Recombinantes/biossíntese , Proteínas Recombinantes/genética , Proteínas Recombinantes/imunologia , Análise de Sequência de DNA , Vacinação
20.
J Virol ; 85(19): 9847-53, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21697481

RESUMO

Japanese encephalitis virus (JEV), a mosquito-borne zoonotic pathogen, is one of the major causes of viral encephalitis worldwide. Previous phylogenetic studies based on the envelope protein indicated that there are four genotypes, and surveillance data suggest that genotype I is gradually replacing genotype III as the dominant strain. Here we report an evolutionary analysis based on 98 full-length genome sequences of JEV, including 67 new samples isolated from humans, pigs, mosquitoes, midges. and bats in affected areas. To investigate the relationships between the genotypes and the significance of genotype I in recent epidemics, we estimated evolutionary rates, ages of common ancestors, and population demographics. Our results indicate that the genotypes diverged in the order IV, III, II, and I and that the genetic diversity of genotype III has decreased rapidly while that of genotype I has increased gradually, consistent with its emergence as the dominant genotype.


Assuntos
Vírus da Encefalite Japonesa (Espécie)/classificação , Vírus da Encefalite Japonesa (Espécie)/genética , Encefalite Japonesa/epidemiologia , Encefalite Japonesa/virologia , Genoma Viral , Animais , Ásia/epidemiologia , Análise por Conglomerados , Vírus da Encefalite Japonesa (Espécie)/isolamento & purificação , Genótipo , Humanos , Dados de Sequência Molecular , Filogenia , RNA Viral/genética , Análise de Sequência de DNA
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