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1.
Gut ; 2021 Nov 26.
Artigo em Inglês | MEDLINE | ID: mdl-34836916

RESUMO

OBJECTIVE: Helicobacter pylori infection is mostly a family-based infectious disease. To facilitate its prevention and management, a national consensus meeting was held to review current evidence and propose strategies for population-wide and family-based H. pylori infection control and management to reduce the related disease burden. METHODS: Fifty-seven experts from 41 major universities and institutions in 20 provinces/regions of mainland China were invited to review evidence and modify statements using Delphi process and grading of recommendations assessment, development and evaluation system. The consensus level was defined as ≥80% for agreement on the proposed statements. RESULTS: Experts discussed and modified the original 23 statements on family-based H. pylori infection transmission, control and management, and reached consensus on 16 statements. The final report consists of three parts: (1) H. pylori infection and transmission among family members, (2) prevention and management of H. pylori infection in children and elderly people within households, and (3) strategies for prevention and management of H. pylori infection for family members. In addition to the 'test-and-treat' and 'screen-and-treat' strategies, this consensus also introduced a novel third 'family-based H. pylori infection control and management' strategy to prevent its intrafamilial transmission and development of related diseases. CONCLUSION: H. pylori is transmissible from person to person, and among family members. A family-based H. pylori prevention and eradication strategy would be a suitable approach to prevent its intra-familial transmission and related diseases. The notion and practice would be beneficial not only for Chinese residents but also valuable as a reference for other highly infected areas.

2.
Pregnancy Hypertens ; 26: 102-109, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34739939

RESUMO

OBJECTIVE: To predict risk of pre-eclampsia (PE) in women using machine learning (ML) algorithms, based on electronic health records (EHR) collected at the early second trimester. STUDY DESIGN: A total of 3759 cases of pregnancy who received antenatal care at Xinhua hospital Chongming branch Affiliated to Shanghai Jiaotong University were included in this retrospective EHR-based study. Thirty-eight candidate clinical parameters routinely available at the first visit in antenatal care were collected by manual chart review. Logistic regression (LR), random forest (RF), support vector machine (SVM) and extreme gradient boosting (XGBoost) were used to construct the prediction model. Features that contributed to the model predictions were identified using XGBoost. OUTCOME MEASURES: The performance of ML models to predict women at risk of PE was quantified in terms of accuracy, precision, recall, false negative score, f1_score, brier score and the area under the receiver operating curve (auROC). RESULTS: The XGboost model had the best prediction performance (accuracy = 0.920, precision = 0.447, recall = 0.789, f1_score = 0.571, auROC = 0.955). The most predictive feature of PE development was fasting plasma glucose, followed by mean blood pressure and body mass index. An easy-to-use model that a patient could answer independently still enabled accurate prediction, with auROC of 0.83. CONCLUSION: risk of PE development can be predicted with excellent discriminative ability using ML algorithms based on EHR collected at the early second trimester. Future studies are needed to assess the real-world clinical utility of the model.

3.
Opt Express ; 29(21): 33245-33256, 2021 Oct 11.
Artigo em Inglês | MEDLINE | ID: mdl-34809140

RESUMO

We theoretically investigate the atomic-orbital-resolved vortex-shaped photoelectron momentum distributions (PMDs) and ionization probabilities by solving the two-dimensional time-dependent Schrödinger equation (2D-TDSE) of neon in a pair of delayed counter-rotating circularly polarized attosecond pulses. We found that the number of spiral arms in vortex patterns is twice the number of absorbed photons when the initial state is the ψm=±1 state, which satisfy a change from c2n+2 to c2n (n is the number of absorbed photons) rotational symmetry of the vortices if the 2p state is replaced by 2p+ or 2p- states. For two- and three-photon ionization, the magnetic quantum number dependence of ionization probabilities is quite weak. Interestingly, single-photon ionization is preferred when the electron and laser field corotate and ionization probabilities of 2p- is much larger than that of 2p+ if the proper time delay and wavelength are used. The relative ratio of ionization probabilities between 2p- and 2p+ is insensitive to laser peak intensity, which can be controlled by changing the wavelength, time delay, relative phase and amplitude ratio of two attosecond pulses.

4.
Biochem Biophys Res Commun ; 578: 7-14, 2021 Nov 12.
Artigo em Inglês | MEDLINE | ID: mdl-34520980

RESUMO

Ubiquitin-conjugating enzyme E2S (UBE2S), an important E2 enzyme in the process of ubiquitination, has exhibited oncogenic activities in various malignant tumors. However, it remains unknown whether UBE2S plays a role in urinary bladder cancer (UBC) development. In the current study, our data confirmed UBE2S upregulation in UBC. In vitro and in vivo experiments demonstrated that UBE2S knockdown resulted in attenuated proliferation and enhanced apoptosis, which was inverse to the phenotypes with UBE2S overexpression. Gain and loss of function assays confirmed that UBE2S exerts oncogenic activities in UBC by mediating the activation of the mammalian target of rapamycin complex 1 (mTORC1) pathway. Furthermore, we discovered that this UBE2S-modulated carcinogenic mechanism was in the consequence of directly targeting tuberous sclerosis 1 (TSC1), which is the upstream inhibitor of mTOR signaling for ubiquitous degradation. Taken together, this study demonstrated that UBE2S is a carcinogen in UBC and promotes UBC progression by ubiquitously degrading TSC1. This consequently mediates the activation of the mTOR pathway, suggesting a potential therapeutic regimen for UBC by targeting the newly identified UBE2S/TSC1/mTOR axis.

5.
J Nanosci Nanotechnol ; 21(12): 6135-6142, 2021 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-34229814

RESUMO

Supported catalysts, consisting of PMo12 immobilized on silver nanomaterials at different recombination time and the silver nanomaterials with different template sodium citrate amount characterized by FT-IR, XRD, SEM, UV-vis and other test methods. The results show that the AgNPs are relatively uniformed with sizes between 100-300 nm when the sodium citrate addition amount is 9.0 mL. As the reaction time of PMo12/AgNPs increases, the adhesion of AgNPs on the surface of PMo12 becomes more complete. Using PMo12 and PMo12/AgNPs composite materials as catalysts, methylene blue (MB) is photocatalytically degraded under simulated visible light conditions. The results show that PMo12 can catalyze MB effectively, and the decolorization rate reached 98.6% when the catalyst content is 2 g/L, the solution pH is 3 and the MB concentration is 5 mg/L. Under the same experimental conditions, photocatalytic performance of the PMo12/AgNPs system is better than that of the PMo12 further improved the photocatalytic degradation effect of the MB solution with a decolorization rate of 100%. The composite still keeps good photocatalytic activity and stability after three cycles of use. Finally, the catalytic mechanism of the POMs composite material is preliminarily discussed.


Assuntos
Azul de Metileno , Prata , Catálise , Espectroscopia de Infravermelho com Transformada de Fourier , Compostos de Tungstênio
6.
Environ Sci Pollut Res Int ; 28(41): 58142-58153, 2021 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-34109523

RESUMO

Recently, increasing attention has been paid to the effects of air pollutants on autoimmune diseases. The results of relationship between ambient air pollution and multiple sclerosis (MS) showed a variety of differences. Thus, the purpose of this study is to further clarify and quantify the relationship between ambient air pollutants and MS through meta-analysis. Through electronic literature search, literature related to our research topic was collected in Cochrane Library, Embase, and PubMed till August 18, 2020, according to certain criteria. Pooled risk estimate and 95% confidence intervals (95%CI) were calculated by random-effect model analysis. After removing copies, browsing titles and abstracts, and reading full text, 6 studies were finally included. The results showed that only particulate matter (PM) with aerodynamic diameter ≤ 10 (PM10) was related to MS (pooled HR = 1.058, 95% CI = 1.050-1.066), and no correlation was found between PM with aerodynamic diameter < 2.5 (PM2.5), nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), benzene (C6H6), major road < 50 m, and MS. There was no publication bias, and the heterogeneity analysis results were stable. PM10 is correlated with the disease MS, while other pollution is not connected with MS. Therefore, it is important for MS patients to take personal protection against particulate pollution and avoid exposure to higher levels of PM.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Esclerose Múltipla , Ozônio , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/análise , Humanos , Dióxido de Nitrogênio/análise , Ozônio/análise , Material Particulado/efeitos adversos , Material Particulado/análise
8.
Aging (Albany NY) ; 12(16): 16099-16110, 2020 08 28.
Artigo em Inglês | MEDLINE | ID: mdl-32855360

RESUMO

Inflammatory bowel disease (IBD) is a group of chronic and recurrent nonspecific inflammatory disorders, including Crohn's disease (CD) and ulcerative colitis (UC). Due to the persistent inflammation of intestinal mucosa caused by immune disorders, barrier dysfunction may be an essential cause of the pathogenesis of IBD. Therefore, exploring the mechanism is very important to clarify the pathogenesis of IBD. In our research, we provided evidence of IL-21 function in IBD. The junction complex protein claudin-5 may be a downstream gene of the IL-21. Anti-IL-21 administrated prevented DSS-simulative colitis via recovering claudin-5 expression in the human colonic epithelial cells. Meanwhile, we described that miR-423-5p could be involved in IL-21/ claudin-5 pathway by regulating NF-κB/MAPKs/JNK signaling pathway, which may provide a new therapeutic target for IBD.


Assuntos
Claudina-5/metabolismo , Colite Ulcerativa/metabolismo , Colite/metabolismo , Colo/metabolismo , Interleucinas/metabolismo , Mucosa Intestinal/metabolismo , MicroRNAs/metabolismo , Animais , Células CACO-2 , Estudos de Casos e Controles , Claudina-5/genética , Colite/induzido quimicamente , Colite/genética , Colite/patologia , Colite Ulcerativa/genética , Colite Ulcerativa/patologia , Colo/patologia , Sulfato de Dextrana , Modelos Animais de Doenças , Impedância Elétrica , Regulação da Expressão Gênica , Humanos , Interleucinas/genética , Mucosa Intestinal/patologia , Camundongos Endogâmicos C57BL , MicroRNAs/genética , Permeabilidade , Transdução de Sinais
9.
Curr Pharm Des ; 26(46): 5998-6006, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32851953

RESUMO

OBJECTIVE: Due to the inconsistent results of current studies on the association between urinary and blood vascular cell adhesion molecule-1 (VCAM-1) and systemic lupus erythematosus (SLE) disease activity, we conducted this study and analyzed its influencing factors. METHODS: A literature search was conducted in PubMed, EMBASE, Web of Science, and Cochrane Library. Data were extracted from eligible studies to calculate standardized mean differences (SMD) with 95% confidence intervals (CI). Cochrane Q test and I2 statistics were used to examine heterogeneity. The sources of heterogeneity were assessed through sensitivity analysis and subgroup analysis. Publication bias was evaluated by funnel plots and Egger's test. RESULTS: A total of 15 studies met the inclusion criteria, including 473 active SLE patients and 674 inactive SLE patients. The random effects model was used for data analysis. In both urine and blood samples, VCAM- 1 level in active SLE patients was significantly higher than those in inactive SLE patients (urine: SMD: 0.769; 95% CI: 0.260-1.278; blood: SMD=0.655, 95% CI: 0.084-1.226). No publication bias was found in this study. CONCLUSION: Compared with inactive SLE patients, patients with active SLE have higher levels of VCAM-1 in both urine and blood. VCAM-1 may be a potential indicator of SLE disease activity.


Assuntos
Lúpus Eritematoso Sistêmico , Molécula 1 de Adesão de Célula Vascular , Biomarcadores , Análise de Dados , Humanos
10.
Mol Psychiatry ; 2020 Jul 17.
Artigo em Inglês | MEDLINE | ID: mdl-32681097

RESUMO

It is traditionally believed that cerebral amyloid-beta (Aß) deposits are derived from the brain itself in Alzheimer's disease (AD). Peripheral cells such as blood cells also produce Aß. The role of peripherally produced Aß in the pathogenesis of AD remains unknown. In this study, we established a bone marrow transplantation model to investigate the contribution of blood cell-produced Aß to AD pathogenesis. We found that bone marrow cells (BMCs) transplanted from APPswe/PS1dE9 transgenic mice into wild-type (Wt) mice at 3 months of age continuously expressed human Aß in the blood, and caused AD phenotypes including Aß plaques, cerebral amyloid angiopathy (CAA), tau hyperphosphorylation, neuronal degeneration, neuroinflammation, and behavioral deficits in the Wt recipient mice at 12 months after transplantation. Bone marrow reconstitution in APPswe/PS1dE9 mice with Wt-BMCs at 3 months of age reduced blood Aß levels, and alleviated brain Aß burden, neuronal degeneration, neuroinflammation, and behavioral deficits in the AD model mice at 12 months after transplantation. Our study demonstrated that blood cell-produced Aß plays a significant role in AD pathogenesis, and the elimination of peripheral production of Aß can decrease brain Aß deposition and represents a novel therapeutic approach for AD.

12.
J Sci Food Agric ; 100(5): 2296-2304, 2020 Mar 30.
Artigo em Inglês | MEDLINE | ID: mdl-31953836

RESUMO

BACKGROUND: The thermal processing of food results in the formation of α-dicarbonyl compounds (α-DCs) such as glyoxal (GO), methylglyoxal (MGO), 2,3-butanedione (2,3-BD), and 3-deoxyglucosone (3-DG), which are precursors of potentially harmful advanced glycation end products. Some of the α-DCs found in food products might result from chemical deterioration reactions during storage and reheating. A range of sugary food simulation systems were stored at three different temperatures (4, 25, and 37 °C) and reheated using three different processing methods to investigate the formation and migration of α-DCs. RESULTS: During 20 days of storage, the concentration of α-DCs declined, following which the concentration remained approximately constant. Methylglyoxal was the major α-DC affected during storage, its relative content decreasing from 233.71 to 44.12 µg mL-1 in the glucose-lysine system. The concentration of α-DCs decreased with increasing temperature. Microwave reheating increased the formation of α-DC compounds. The largest increases in 3-DG concentrations were observed in the maltose-lysine systems (24.94 to 35.74 µg mL-1 ). The concentration of α-DCs only changed a little in response to reheating at 100 °C, but declined when reheated at 150 °C. CONCLUSION: The concentration of α-DCs following storage and reheating depends on the type of sugar, lysine content, temperature, and method of reheating. © 2020 Society of Chemical Industry.


Assuntos
Desoxiglucose/análise , Diacetil/análise , Produtos Finais de Glicação Avançada/análise , Glioxal/análise , Temperatura Alta , Aldeído Pirúvico/análise , Carboidratos , Desoxiglucose/análogos & derivados , Alimentos , Análise de Alimentos , Armazenamento de Alimentos , Glucose , Lisina , Temperatura
13.
Clin Rheumatol ; 39(1): 281-290, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31523787

RESUMO

OBJECTIVES: CXC ligand 13 (CXCL13) is known as B cell chemotactic factor (BLC), promoting the migration of B lymphocytes by communicating with its receptor CXCR5, which can be regarded as part of pathogenesis of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). This meta-analysis was to evaluate the circulating CXCL13 levels in SLE and RA. METHODS: All articles were respectively gathered from PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) (by the end of 10 April 2019). According to random effects model, standardized mean difference (SMD) and 95% confidence interval (CI) of CXCL13 levels in SLE and RA were calculated by Stata 12.0 software. RESULTS: Totally, 15 studies were selected (981 SLE patients and 380 healthy controls, 332 RA patients and 147 healthy controls). SLE and RA patients were significantly increased in circulating CXCL13 levels (SMD = 1.851, 95% CI 0.604-3.098; SMD = 1.801, 95% CI = 1.145-2.457). Subgroup analyses showed that SLE patients from the Chinese group and systemic lupus erythematosus disease activity index (SLEDAI) score ≥ 6 group had higher circulating CXCL13 levels (SMD = 2.182, 95% CI 0.135-4.229; SMD = 0.767, 95% CI 0.503-1.030). However, there were no significant changes in CXCL13 concentrations in SLE patients from the English and SLEDAI score < 6 group. Similarly, subgroup analyses presented that RA patients from different classifications showed higher circulating CXCL13 levels. There was no publication bias. CONCLUSIONS: This meta-analysis demonstrated increased circulating CXCL13 concentrations in SLE and RA patients. Circulating CXCL13 levels may act as biomarkers and therapy targets in the diagnosis and treatment of SLE and RA.Key Point• First, CXC ligand 13 (CXCL13) is closely related to the pathogenesis of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), Second, this study may provide novel therapeutic targets for the treatment of SLE and RA patients. This meta-analysis provides a comprehensive analysis of circulating CXCL13 levels in patients with SLE and RA and also explores related influencing factors.


Assuntos
Artrite Reumatoide/sangue , Quimiocina CXCL13/sangue , Lúpus Eritematoso Sistêmico/sangue , Artrite Reumatoide/fisiopatologia , Biomarcadores/sangue , Humanos , Lúpus Eritematoso Sistêmico/fisiopatologia
14.
World J Gastroenterol ; 25(43): 6386-6403, 2019 Nov 21.
Artigo em Inglês | MEDLINE | ID: mdl-31798276

RESUMO

BACKGROUND: Hepatocellular carcinoma (HCC) is now the most common primary liver malignancy worldwide, and multiple risk factors attribute to the occurrence and development of HCC. Recently, increasing studies suggest that ubiquitin-conjugating enzyme E2T (UBE2T) serves as a promising prognostic factor in human cancers, although the molecular mechanism of UBE2T in HCC remains unclear. AIM: To investigate the clinical relevance and role of UBE2T in HCC development. METHODS: UBE2T expression in HCC tissues from the TCGA database and its association with patient survival were analyzed. A lentivirus-mediated strategy was used to knock down UBE2T in HCC cells. qRT-PCR and Western blot assays were performed to check the effect of UBE2T silencing in HCC cells. Cell growth in vitro and in vivo was analyzed by multiparametric high-content screening and the xenograft tumorigenicity assay, respectively. Cell cycle distribution and apoptosis were determined by flow cytometry. The genes regulated by UBE2T were profiled by microarray assay. RESULTS: UBE2T was overexpressed in HCC tissues compared with paired and non-paired normal tissues. High expression of UBE2T predicted a poor overall survival in HCC patients. In vitro, lentivirus-mediated UBE2T knockdown significantly reduced the viability of both SMMC-7721 and BEL-7404 cells. In vivo, the xenograft tumorigenesis of SMMC-7721 cells was largely attenuated by UBE2T silencing. The cell cycle was arrested at G1/S phase in SMMC-7721 and BEL-7404 cells with UBE2T knockdown. Furthermore, apoptosis was increased by UBE2T knockdown. At the molecular level, numerous genes were dysregulated after UBE2T silencing, including IL-1B, FOSL1, PTGS2, and BMP6. CONCLUSION: UBE2T plays an important role in cell cycle progression, apoptosis, and HCC development.


Assuntos
Carcinogênese , Carcinoma Hepatocelular/enzimologia , Neoplasias Hepáticas/enzimologia , Oncogenes , Enzimas de Conjugação de Ubiquitina/metabolismo , Apoptose , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/mortalidade , Ciclo Celular , Linhagem Celular Tumoral , Técnicas de Silenciamento de Genes , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/mortalidade , Enzimas de Conjugação de Ubiquitina/genética
15.
World J Gastroenterol ; 25(41): 6222-6237, 2019 Nov 07.
Artigo em Inglês | MEDLINE | ID: mdl-31749593

RESUMO

BACKGROUND: Pediatric enteritis is one of the infectious diseases in the digestive system that causes a variety of digestive problems, including diarrhea, vomiting, and bellyache in children. Clinically, Helicobacter pylori (H. pylori) infection is one of the common factors to cause pediatric enteritis. It has been demonstrated that aberrant expression of microRNAs (miRNAs) is found in gastrointestinal diseases caused by H. pylori, and we discovered a significant increase of miR-32-5p in H. pylori-related pediatric enteritis. However, the exact role of miR-32-5p in it is still unknown. AIM: To investigate the role of aberrant miR-32-5p in pediatric enteritis induced by H. pylori. METHODS: MiR-32-5p expression was detected by quantitative real time-polymerase chain reaction. The biological role of miR-32-5p in H. pylori-treated intestinal epithelial cells was evaluated by Cell Counting Kit-8 assay and flow cytometry. The potential target of miR-32-5p was predicted with TargetScanHuman and verified by luciferase assay. The downstream mechanism of miR-32-5p was explored by using molecular biology methods. RESULTS: We found that miR-32-5p was overexpressed in serum of H. pylori-induced pediatric enteritis. Further investigation revealed that H. pylori infection promoted the death of intestinal epithelial cells, and increased miR-32-5p expression. Moreover, miR-32-5p mimic further facilitated apoptosis and inflammatory cytokine secretion of intestinal epithelial cells. Further exploration revealed that SMAD family member 6 (SMAD6) was the direct target of miR-32-5p, and SMAD6 overexpression partially rescued cell damage induced by H. pylori. The following experiments showed that miR-32-5p/SMAD6 participated in the apoptosis of intestinal epithelial cells induced by transforming growth factor-ß-activated kinase 1 (TAK1)-p38 activation under H. pylori infection. CONCLUSION: Our work uncovered the crucial role of aberrant expression of miR-32-5p in H. pylori-related pediatric enteritis, and suggested that the TAK1-p38 pathway is involved in it.


Assuntos
Enterite/patologia , Células Epiteliais/patologia , Infecções por Helicobacter/metabolismo , Helicobacter pylori/patogenicidade , MicroRNAs/metabolismo , Dor Abdominal/microbiologia , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Apoptose , Estudos de Casos e Controles , Sobrevivência Celular , Criança , Citocinas/metabolismo , Diarreia/microbiologia , Enterite/microbiologia , Células Epiteliais/microbiologia , Citometria de Fluxo , Regulação da Expressão Gênica , Células HEK293 , Infecções por Helicobacter/microbiologia , Humanos , Inflamação , Intestinos , RNA Interferente Pequeno/metabolismo , Proteína Smad6/metabolismo , Vômito/microbiologia , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
16.
Med Sci Monit ; 25: 5594-5605, 2019 Jul 28.
Artigo em Inglês | MEDLINE | ID: mdl-31352465

RESUMO

BACKGROUND We previously reported that cerebellar fastigial nucleus stimulation reduced post-stroke depression in a rat model by reducing inflammation. This study aimed to investigate the molecular inflammatory signaling pathways associated with cerebellar fastigial nucleus stimulation in an established rat model of post-stroke depression. MATERIAL AND METHODS Twenty-four Sprague-Dawley rats included a sham group (N=6), an untreated stroke group (N=6), an untreated post-stroke depression model group (PSD) (N=6), and the model group treated with cerebellar fastigial nucleus stimulation (FNS) (N=6). The rat stroke model involved occlusion of the middle cerebral artery occlusion (MCAO). Post-stroke depression model was established using chronic unpredictable mild stress treatment and was verified using an open field test. Real-time polymerase chain reaction (PCR) and Western blot compared expression levels of microRNA-29c (miR-29c), miR-676, TNFRSF1A, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 and IL-1ß in cerebellar tissue. U251 human glioblastoma cells and SH-SY5Y human neuroblastoma cells were studied in vitro. RESULTS Cerebellar fastigial nucleus stimulation reduced behaviors associated with depression in the rat model, upregulated the expression of miR-29c, and reduced the expression of TNFRSF1A and inflammatory cytokines, and mildly reduced neuronal apoptosis. Bioinformatics data analysis identified a regulatory relationship between miR-29c and TNFRSF1A. SH-SY5Y cells treated with a miR-29c mimic, or TNFRSF1A short interfering RNA (siRNA), identified a negative regulatory relationship between TNFRSF1A and miR-29c. CONCLUSIONS In a rat model, cerebellar fastigial nucleus stimulation reduced the expression of TNFRSF1A by upregulating miR-29c expression, which suppressed the expression of inflammatory cytokines, resulting in reduced severity of post-stroke depression.


Assuntos
Núcleos Cerebelares/fisiologia , MicroRNAs/genética , Animais , Apoptose , Isquemia Encefálica/metabolismo , Linhagem Celular , Núcleos Cerebelares/metabolismo , Estimulação Encefálica Profunda/métodos , Depressão/fisiopatologia , Transtorno Depressivo/complicações , Transtorno Depressivo/metabolismo , Modelos Animais de Doenças , Encefalite/complicações , Humanos , Infarto da Artéria Cerebral Média/complicações , Inflamação/genética , Inflamação/metabolismo , MicroRNAs/metabolismo , Ratos , Ratos Sprague-Dawley , Receptores Tipo I de Fatores de Necrose Tumoral/genética , Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo , Transdução de Sinais/genética , Estresse Fisiológico/fisiologia , Acidente Vascular Cerebral/complicações
17.
Chin Med J (Engl) ; 132(13): 1610-1614, 2019 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-31090547

RESUMO

OBJECTIVE: The metabolites produced by the gut microbiota are of interest to scientists. The objective of this review was to provide an updated summary of progress regarding the microbiota and their metabolites and influences on the pathogenesis of inflammatory bowel disease (IBD). DATA SOURCES: The author retrieved information from the PubMed database up to January 2018, using various combinations of search terms, including IBD, microbiota, and metabolite. STUDY SELECTION: Both clinical studies and animal studies of intestinal microbiota and metabolites in IBD were selected. The information explaining the possible pathogenesis of microbiota in IBD was organized. RESULTS: In IBD patients, the biodiversity of feces/mucosa-associated microbiota is decreased, and the probiotic microbiota is also decreased, whereas the pathogenic microbiota are increased. The gut microbiota may be a target for diagnosis and treatment of IBD. Substantial amounts of data support the view that the microbiota and their metabolites play pivotal roles in IBD by affecting intestinal permeability and the immune response. CONCLUSIONS: This review highlights the advances in recent gut microbiota research and clarifies the importance of the gut microbiota in IBD pathogenesis. Future research is needed to study the function of altered bacterial community compositions and the roles of metabolites.


Assuntos
Microbioma Gastrointestinal/fisiologia , Doenças Inflamatórias Intestinais/metabolismo , Doenças Inflamatórias Intestinais/microbiologia , Animais , Fezes/microbiologia , Humanos , Intestinos/microbiologia , Microbiota/fisiologia , Probióticos
18.
J Sci Food Agric ; 99(2): 790-796, 2019 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-29998459

RESUMO

BACKGROUND: In the present study, we investigated the role of ornithine decarboxylase (ODC) in the methyl jasmonate (MeJA)-regulated postharvest quality maintenance of Agaricus bisporus (J. E. Kange) Imbach button mushrooms by pretreating mushrooms with a specific irreversible inhibitor called α-difluoromethylornithine (DFMO) before exposure to MeJA vapor. RESULTS: Mushrooms were treated with 0 or 100 µmol L-1 MeJA or a combination of 120 µmol L-1 DFMO and 100 µmol L-1 MeJA, respectively, before storage at 4 °C for 21 days. Treatment with MeJA alone induced the increase in ODC activity whereas this effect was greatly suppressed by pretreatment with DFMO. α-Difluoromethylornithine strongly attenuated the effect of MeJA on decreasing cap opening, slowing the decline rate of soluble protein and total sugar, and accumulating total phenolics and flavonoids. α-Difluoromethylornithine pretreatment also counteracted the ability of MeJA to inhibit polyphenol oxidase and lipoxygenase activities, and malondialdehyde production, and to stimulate superoxide dismutase and catalase activities. It also largely downregulated MeJA-induced accumulation of free putrescine (Put). CONCLUSION: These results reveal that ODC is involved in MeJA-regulated postharvest quality retention of button mushrooms, and this involvement is likely to be associated with Put levels. © 2018 Society of Chemical Industry.


Assuntos
Acetatos/farmacologia , Agaricus/química , Agaricus/efeitos dos fármacos , Ciclopentanos/farmacologia , Proteínas Fúngicas/metabolismo , Ornitina Descarboxilase/metabolismo , Oxilipinas/farmacologia , Agaricus/enzimologia , Agaricus/crescimento & desenvolvimento , Catecol Oxidase/metabolismo , Flavonoides/análise , Flavonoides/metabolismo , Malondialdeído/metabolismo , Fenóis/análise , Fenóis/metabolismo , Putrescina/análise , Putrescina/metabolismo , Controle de Qualidade , Superóxido Dismutase/metabolismo
19.
Chin Med J (Engl) ; 131(18): 2152-2157, 2018 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-30203788

RESUMO

Background: Whether the Glasgow Coma Scale (GCS) can assess intubated patients is still a topic of controversy. We compared the test performance of the GCS motor component (GCS-M)/Simplified Motor Score (SMS) to the total of the GCS in predicting the outcomes of intubated acute severe cerebral vascular disease patients. Methods: A retrospective analysis of prospectively collected observational data was performed. Between January 2012 and October 2015, 106 consecutive acute severe cerebral vascular disease patients with intubation were included in the study. GCS, GCS-M, GCS eye-opening component, and SMS were documented on admission and at 24, 48, and 72 h after admission to Neurointensive Care Unit (NCU). Outcomes were death and unfavorable prognosis (modified Rankin Scale: 5-6) at NCU discharge. The receiver operating characteristic (ROC) curve was obtained to determine the prognostic performance and best cutoff value for each scoring system. Comparison of the area under the ROC curves (AUCs) was performed using the Z- test. Results: Of 106 patients included in the study, 41 (38.7%) patients died, and 69 (65.1%) patients had poor prognosis when discharged from NCU. The four time points within 72 h of admission to the NCU were equivalent for each scale's predictive power, except that 0 h was the best for each scale in predicting outcomes of patients with right-hemisphere lesions. Nonsignificant difference was found between GCS-M AUCs and GCS AUCs in predicting death at 0 h (0.721 vs. 0.717, Z = 0.135, P = 0.893) and 72 h (0.730 vs. 0.765, Z = 1.887, P = 0.060), in predicting poor prognosis at 0 h (0.827 vs. 0.819, Z = 0.395, P = 0.693), 24 h (0.771 vs. 0.760, Z = 0.944, P = 0.345), 48 h (0.732 vs. 0.741, Z = 0.593, P = 0.590), and 72 h (0.775 vs. 0.780, Z = 0.302, P = 0.763). AUCs in predicting death for patients with left-hemisphere lesions ranged from 0.700 to 0.804 for GCS-M and from 0.700 to 0.824 for GCS, in predicting poor prognosis ranged from 0.841 to 0.969 for GCS-M and from 0.875 to 0.969 for GCS, with no significant difference between GCS-M AUCs and GCS AUCs within 72 h (P > 0.05). No significant difference between GCS-M AUCs and GCS AUCs was found in predicting death (0.964 vs. 0.964, P = 1.000) and poor prognosis (1.000 vs. 1.000, P = 1.000) for patients with right-hemisphere lesions at 0 h. AUCs in predicting death for patients with brainstem or cerebella were poor for GCS-M (<0.700), in predicting poor prognosis ranged from 0.727 to 0.801 for GCS-M and from 0.704 to 0.820 for GCS, with no significant difference between GCS-M AUCs and GCS AUCs within 72 h (P > 0.05). The SMS AUCs (<0.700) in predicting outcomes were poor. Conclusions: The GCS-M approaches the same test performance as the GCS in assessing the prognosis of intubated acute severe cerebral vascular disease patients. The GCS-M could be accurately and reliably applied in patients with hemisphere lesions, but caution must be taken for patients with brainstem or cerebella lesions.


Assuntos
Coma/diagnóstico , Escala de Coma de Glasgow , Intubação Intratraqueal , Acidente Vascular Cerebral/complicações , Adolescente , Adulto , Coma/etiologia , Humanos , Prognóstico , Estudos Retrospectivos
20.
Oncol Lett ; 15(5): 7963-7972, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29849802

RESUMO

Non-coding RNAs are important in the progression of liver cancer. The present study aimed to investigate the effects of long non-coding RNA HOX transcript antisense RNA (HOTAIR) on the proliferation of liver cancer and the association between HOTAIR and microRNA (miR)-217. It was demonstrated that the expression of HOTAIR was upregulated in liver cancer tissues and 3 liver cancer cell lines (MHCC97H, HepG2 and Hep3B). Inhibition of HOTAIR with HOTAIR small interfering (si) RNA lentiviral vectors significantly suppressed the cell proliferation of HepG2 cells, and downregulated the protein expression levels of two proliferation markers, Ki67 and proliferating cell nuclear antigen (PCNA). Furthermore, inhibition of HOTAIR induced G0/G1 cycle arrest by increasing the expression of p27 and decreasing the expression of cyclin D1. It was then predicted and verified that miR-217 was the target of HOTAIR. Expression of miR-217 was downregulated in liver cancer tissues and the 3 liver cancer cell lines. Further results revealed that inhibition of HOTAIR markedly upregulated the expression of miR-217 in HepG2 cells, and miR-217 inhibitor-induced reduction of miR-217 was significantly suppressed by HOTAIR inhibition. Furthermore, the increased cell proliferation and growth, the upregulated expression of Ki67 and PCNA, and the reduced G0/G1 cycle arrest induced by miR-217 inhibitor were partly rescued by inhibition of HOTAIR. Finally, the in vivo experiment indicated that HOTAIR inhibition suppressed tumorigenesis, including the smaller tumor volume and the reduced levels of Ki67. Overall, HOTAIR contributes to the proliferation and growth of liver cancer via downregulation of miR-217.

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