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Fluorescence in situ hybridization (FISH) is a powerful technique used for detecting and localizing specific nucleic acid sequences in cells or tissues. Double-stranded RNA (dsRNA) is a type of RNA with complementary strands, highly produced during the replication cycle of RNA viruses. dsRNA plays an essential role in many biological processes, including the activation of RNA silencing. Here, we present an overview of how FISH can be employed to detect and locate dsRNA. The detection and localization of dsRNA through FISH provide valuable insights into RNA-mediated processes and their roles in various biological phenomena.
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RNA de Cadeia Dupla , RNA de Cadeia Dupla/genética , Hibridização in Situ Fluorescente , Interferência de RNARESUMO
The autophagic degradation of lipid droplets, termed lipophagy, is the main mechanism contributing to lipid consumption in hepatocytes. Identifying effective and safe natural compounds that target lipophagy to eliminate excess lipids may be a potential therapeutic strategy for non-alcoholic fatty liver disease (NAFLD). Here the effects of naringin on NAFLD and the underlying mechanisms involved are investigated. Naringin treatment effectively relieves HFD-induced hepatic steatosis in mice and inhibits PA-induced lipid accumulation in hepatocytes. Increased p62 and LC3-II levels are observed with excess lipid support autophagosome accumulation and impaired autophagic flux. Treatment with naringin restores TFEB-mediated lysosomal biogenesis, thereby promoting the fusion of autophagosomes and lysosomes, restoring impaired autophagic flux and further inducing lipophagy. However, the knockdown of TFEB in hepatocytes or the hepatocyte-specific knockout of TFEB in mice abrogates naringin-induced lipophagy, eliminating its therapeutic effect on hepatic steatosis. These results demonstrate that TFEB-mediated lysosomal biogenesis and subsequent lipophagy play essential roles in the ability of naringin to mitigate hepatic steatosis and suggest that naringin is a promising drug for treating NAFLD.
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Flavanonas , Hepatopatia Gordurosa não Alcoólica , Camundongos , Animais , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Hepatopatia Gordurosa não Alcoólica/metabolismo , Hepatócitos , Autofagia , Lipídeos/farmacologia , Fígado/metabolismoRESUMO
Paper-based friction material is a typical paper-based composite that is usually cured via hot-pressing. This curing method does not account for the effect of pressure on the matrix resin, resulting in uneven distribution of resin in the material and reducing the mechanical properties of friction materials. To overcome the above shortcomings, a pre-curing method was introduced before hot-pressing, and the effects of different pre-curing degrees on the surface morphology and mechanical properties of paper-based friction materials were studied. The pre-curing degree significantly affected the resin distribution and interfacial bonding strength of the paper-based friction material. When the material was cured at 160 °C for 10 min, the pre-curing degree reached 60%. At this point, most of the resin was in a gel state, which could retain abundant pore structures on the material surface without causing mechanical damage to the fiber and resin matrix during hot-pressing. Ultimately, the paper-based friction material exhibited improved static mechanical properties, decreased permanent deformation, and reasonable dynamic mechanical properties.
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Robust plant immune systems are fine-tuned by both protein-coding genes and non-coding RNAs. Long non-coding RNAs (lncRNAs) refer to RNAs with a length of more than 200 nt and usually do not have protein-coding function and do not belong to any other well-known non-coding RNA types. The non-protein-coding, low expression, and non-conservative characteristics of lncRNAs restrict their recognition. Although studies of lncRNAs in plants are in the early stage, emerging studies have shown that plants employ lncRNAs to regulate plant immunity. Moreover, in response to stresses, numerous lncRNAs are differentially expressed, which manifests the actions of low-expressed lncRNAs and makes plant-microbe/insect interactions a convenient system to study the functions of lncRNAs. Here, we summarize the current advances in plant lncRNAs, discuss their regulatory effects in different stages of plant immunity, and highlight their roles in diverse plant-microbe/insect interactions. These insights will not only strengthen our understanding of the roles and actions of lncRNAs in plant-microbe/insect interactions but also provide novel insight into plant immune responses and a basis for further research in this field.
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RNA Longo não Codificante , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Imunidade Vegetal/genética , Regulação da Expressão Gênica de Plantas , RNA de Plantas/genéticaRESUMO
Microplastic pollution in sugarcane areas of China is severe, and reducing the ecological risks is critical. Biochar has been widely used in soil remediation. This study aims to explore the effects and mechanisms of microplastics combined with or without biochar on sugarcane biomass, soil biochemical properties in red soil through a potted experiment. The results show that, compared with control (CK), treatments with microplastics alone reduced the dry biomass of sugarcane, soil pH, and nitrogen (N) and phosphorus (P) contents by an average of 8.8%, 2.1%, 1.1%, and 2.0%, respectively. Interestingly, microplastics combined with biochar could alleviate the negative effects of microplastic accumulation on sugarcane growth and soil quality. There were significant differences in the bacterial community alpha diversity indices and compositions among different treatments. Compared with CK, treatments with microplastics alone obviously decreased the observed operational taxonomic units (OTUs) and the Chao1 and Shannon indices of soil total bacteria (16S rRNA gene-based bacteria) while increasing them in phoD-harboring bacteria. Microplastics combined with biochar treatments significantly increased the abundance of Subgroup_10 for the 16S rRNA gene and treatments with microplastics alone significantly increased the relative abundance of Streptomyces for the phoD gene compared to CK. Moreover, compared with microplastics alone, the treatments with microplastics combined with biochar increased the relative abundance of Subgroup_10, Bacillus, Pseudomonas in soil total bacteria, and Amycolatopsis and Bradyrhizobium in phoD-harboring bacteria, most of which can inhibit harmful bacteria and promote plant growth. Additionally, different treatments also changed the abundance of potential microbial functional genes. Compared to CK, other treatments increased the abundance of aerobic ammonia oxidation and denitrification but decreased the abundance of nitrate respiration and nitrogen respiration; meanwhile, these four functional genes involved in N cycling processes were obviously higher in treatments with microplastics combined with biochar than in treatments with microplastics alone. In conclusion, microplastics combined with biochar could alleviate the negative effects of microplastic accumulation on sugarcane biomass by altering soil nutrients and microbial community structure and function.
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The application of phosphorus (P) fertilizer effectively improves soil P availability, but it also affects soil microbial communities. However, the responses of soil bacterial communities and P forms to long-term P fertilization, and the relationships of bacterial communities with soil P forms remain unclear in P-deficient field. In this study, the impacts of different P fertilization treatments (chemical nitrogen and potassium (NK); chemical N, P and K (NPK); and NPK plus straw (NPKS)) on the bacterial communities and P forms in sugarcane rhizosphere (RS) and bulk soils (BS) were evaluated. Compared with the NK, the NPK and NPKS treatments significantly (P<0.05) increased the yield and quality characters of sugarcane, especially under NPKS. Additionally, P fertilization significantly increased the available P (AP), soluble inorganic P (Pi) and retained Pi in both the RS and BS, but they significantly increased the Chao1 and Shannon index only in the BS; and almost all these indices were significantly higher in the RS than in the BS. The bacterial community compositions were also significantly altered by P fertilization, with major changes in the RS and minor changes in the BS. The bacterial genera that were enriched in the sugarcane rhizosphere mainly included Bradyrhizobium, Rhodanobacter, Pseudolabrys, Conexibacter, and Burkholderia-Caballeronia-Paraburkholderia, some of which potentially promote the plant growth. Compared to NK, functional groups involved in the cycling of carbon, N, and sulfur significantly increased or decreased with fertilizer P application. Moreover, the relative abundances of many bacterial species were significantly correlated with the soil P forms. In conclusion, long-term P fertilization altered bacterial structure and functions in P-deficient sugarcane soil, which could help the soil P cycling and suppling. The results provide useful information to stimulate the power of the microbes by fertilization measures to improve soil nutrients and crop production.
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BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a major clinical and public health burden worldwide with no established pharmacological therapy. Changes in the intestinal flora and associated metabolite bile acids (BAs) have been described in NAFLD. Astragaloside IV (AS-IV) is a low drug permeability saponin with protective effects against multiple diseases. However, the specific mechanism underlying the involvement of AS-IV in the regulation of NAFLD is yet to be clarified. PURPOSE: This study aimed to investigate the effect of AS-IV on NAFLD and explore whether intestinal flora was involved. METHODS: The effect of AS-IV was evaluated on high-fat diet-fed mice. Real-time PCR, immunohistochemistry, immunofluorescence, and biochemical analyses were performed. 16S rRNA gene sequencing and UPLC-TQMS were used to determine the alterations in the intestinal flora and concentration of BAs. Fecal microbiota transplantation (FMT) and intestine-specific farnesoid X receptor (FXR) knockout were also performed. RESULTS: AS-IV treatment alleviated diet-induced metabolic impairments, particularly hepatic steatosis. These changes occurred in the setting of decreased intestinal bile salt hydrolase (BSH)-expressing flora. Further analysis showed that the reduced BSH activity increased intestinal tauro-ß-muricholic acid levels, an inhibitor of intestinal FXR. Inhibition of intestinal FXR signaling by AS-IV was accompanied by decreased expression of intestinal fibroblast growth factor 15 and subsequent hepatic FXR activation as well as increased glucagon-like peptide-1 and decreased ceramide production, all of which contribute to the inhibition of sterol regulatory element-binding protein-1c-mediated hepatic steatosis. Furthermore, intestine-specific Fxr knockout and FMT further demonstrated an FXR- and intestinal flora-dependent preventive effect of AS-IV on hepatic steatosis. CONCLUSION: These results show that the changes in intestinal flora and BAs serve an essential role in the remission of hepatic steatosis by AS-IV, thereby suggesting that AS-IV may be used as a prebiotic agent to provide viable treatment for NAFLD.
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Microbioma Gastrointestinal , Hepatopatia Gordurosa não Alcoólica , Saponinas , Animais , Ácidos e Sais Biliares/metabolismo , Ceramidas/metabolismo , Ceramidas/farmacologia , Dieta Hiperlipídica/efeitos adversos , Fatores de Crescimento de Fibroblastos/metabolismo , Peptídeo 1 Semelhante ao Glucagon/metabolismo , Intestinos , Fígado , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Obesos , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Hepatopatia Gordurosa não Alcoólica/metabolismo , RNA Ribossômico 16S , Receptores Citoplasmáticos e Nucleares/metabolismo , Saponinas/metabolismo , Saponinas/farmacologia , Esteróis/metabolismo , TriterpenosRESUMO
BACKGROUND: Lipophagy is an autophagic process, which delivers the intracellular lipid droplets to the lysosomes for degradation. Recent studies revealed that the impairment of lysosomal biogenesis and autophagic flux led to dysregulation of lipophagy in hepatocytes, which exacerbated the development of nonalcoholic fatty liver disease (NAFLD). Therefore, agents restoring autophagic flux and lipophagy in hepatocytes may have therapeutic potential against this increasingly prevalent disease. Phillygenin (PHI), a lignin extracted from Forsythia suspense, exerts hepatoprotective and anti-inflammatory effects. However, the effect of PHI on NAFLD remains unknown. PURPOSE: This study aimed to investigate the protective effect of PHI on NAFLD and elucidate the underlying mechanism. METHODS: The effects of PHI were examined in palmitate (PA)-stimulated AML12 cells and primary hepatocytes, as well as in NAFLD mice induced by a high-fat diet (HFD). We also used transcription factor EB (TFEB) knockdown hepatocytes and hepatocyte-specific TFEB knockout (TFEBΔhep) mice for mechanistic studies. In vivo and in vitro studies were performed using western blots, immunofluorescence techniques, and transmission electron microscopy. RESULTS: Our results indicated that autophagic flux and lysosome biogenesis in PA-stimulated hepatocytes were impaired. PHI alleviated lipid deposition by increasing lysosomal biogenesis and autophagic flux. It also stimulated the release of endoplasmic reticulum Ca2+ to activate calcineurin, which regulated TFEB dephosphorylation and nuclear translocation, and promoted lysosomal biogenesis. In addition, PHI blocked the NLRP3 inflammasome pathway and improved hepatocyte inflammation in an autophagy-dependent manner. Consistent with the in vitro results, PHI improved hepatic steatosis and inflammation in HFD mice, but these beneficial effects were eliminated in hepatocyte-specific TFEB knockout mice. CONCLUSION: Despite PHI has been reported to have anti-hepatic fibrosis effects, whether it has a hepatoprotective effects against NAFLD and the underlying molecular mechanism remain unclear. Herein, we found that PHI restored lipophagy and suppressed lipid accumulation and inflammation by regulating the Ca2+-calcineurin-TFEB axis in hepatocytes. Thus, PHI represents a therapeutic candidate for the treatment of NAFLD.
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Hepatopatia Gordurosa não Alcoólica , Animais , Autofagia , Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/metabolismo , Calcineurina/metabolismo , Calcineurina/farmacologia , Calcineurina/uso terapêutico , Hepatócitos , Inflamação/metabolismo , Lignanas , Lipídeos , Lisossomos , Camundongos , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Hepatopatia Gordurosa não Alcoólica/metabolismoRESUMO
Quercetin, a natural flavonoid, has been reported to prevent pancreatic ß-cell apoptosis in animal models of diabetes. However, the underlying mechanism remains unclear. We investigated the mechanisms through which quercetin protects ß cells from palmitate-induced apoptosis and determined whether autophagy is involved in this process. We found that quercetin treatment partially reduced palmitate-induced ß-cell apoptosis. This protective effect was abolished by pharmacologic inhibition of autophagy and by silencing a key autophagy gene. Further analysis revealed that palmitate treatment promoted the expression of LC3 II, a marker of autophagosomes, but resulted in the blockade of autophagic flux due to lysosome dysfunction. Defective lysosome accumulation can cause lysosomal membrane permeabilization and the release of cathepsins from lysosome into the cytosol that triggers apoptosis. Treatment with quercetin reversed lysosomal dysfunction and promoted autophagosome-lysosome fusion, which restored defective autophagic flux and provoked autophagy. Overall, our results indicate that lysosomal dysfunction is a major factor that contributes to ß-cell apoptosis and demonstrates that quercetin improves cell survival by restoring lysosomal function and autophagic flux. This study provides new evidence regarding the anti-apoptotic mechanism of quercetin in the treatment of type 2 diabetes.
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Diabetes Mellitus Tipo 2 , Palmitatos , Animais , Apoptose , Autofagia , Diabetes Mellitus Tipo 2/metabolismo , Lisossomos , Palmitatos/metabolismo , Palmitatos/farmacologia , Quercetina/metabolismo , Quercetina/farmacologiaRESUMO
SCOPE: Intestinal flora plays a critical role in the development of . Rutin is a natural flavonoid with potential prebiotic effects on regulating the intestinal flora composition that is beneficial for host health. Therefore, this study hypothesizes that rutin supplementation has beneficial effects on high-fat-diet (HFD)-induced obesity and metabolic disorder through the modulation of intestinal flora in mice. METHODS AND RESULTS: The obesity-alleviating property of rutin using 6-week-old C57BL/6J male mice fed on HFD with or without rutin supplementation for 16 weeks is investigated. Rutin supplementation effectively reduces body-weight gain, insulin resistance, and acted favorably on the intestinal barrier, thereby reducing endotoxemia and systemic inflammation. Sequencing of 16S rRNA genes from fecal samples indicate that rutin exerted modulatory effects on HFD-induced intestinal flora disorders (e.g., rutin decreased Firmicutes abundance and increased Bacteroidetes and Verrucomicrobia abundance). Antibiotic treatment and fecal microbiota transplantation further demonstrate that the salutary effects of rutin on obesity control are strongly dependent on the intestinal flora. CONCLUSION: Rutin can be considered as a prebiotic agent for improving intestinal flora disorders and obesity-associated metabolic perturbations in obese individuals.
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Microbioma Gastrointestinal , Animais , Dieta Hiperlipídica/efeitos adversos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Obesidade/tratamento farmacológico , Obesidade/metabolismo , RNA Ribossômico 16S/genética , Rutina/farmacologiaRESUMO
Seaweed extracts (SEs) have been widely used as biostimulants in crop management due to their growth-promoting and stress-resistant effects. To date, there are few reports of the effect of SEs on sucrose content and cane yield. Here, we conducted field experiments for three consecutive growth seasons (2017â¼2019) in two areas (Suixi and Wengyuan) of China, to investigate the yield and sugar content of sugarcane in response to SE treatment at different growth stages. The results showed that spraying SEs once at seedling (S), early elongation (E), and early mature (M) stages, respectively, once at S and E stages, respectively, or once at the S stage increased the cane yield by 9.23, 9.01, and 3.33%, respectively, implying that SEs application at the early elongation stage played a vital role in promoting sugarcane growth. Photosynthetic parameters and nutrient efficiency analysis showed that spraying SEs at S and E stages enhanced the net photosynthetic rate, transpiration rate, and water use efficiency, and increased N, P, or K utilization efficiency, compared with those of the control. Notably, cane yield increasing rate of SEs in 2017 and 2018 were higher than those in 2019 in Wengyuan but lower than those in 2019 in Suixi. Interestingly, the total rainfall and monthly average rainfall in 2017 and 2018 were lower than those in 2019 in Wengyuan but higher than those in 2019 in Suixi. The results suggested that the yield increasing rate of SEs on sugarcane was better in less rainfall years. The sucrose content of sugarcane showed no difference between spraying SEs at the M stage alone or at the three growth stages but was higher than those of SE treatments at S and/or E stages. Enzyme activity analysis showed that spraying SEs at the M stage increased the activity of sucrose phosphate synthase activity by 9.14% in leaves and 15.16% in stems, and decreased soluble acid invertase activity in stems by 16.52%, which contributed to the sucrose increase of 5.00%. The above results suggested that SEs could increase cane yield and promote sucrose accumulation in sugarcane. The yield increasing effect was more obvious under conditions of drought stress.
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The gut microbiota, often viewed as a "digestive organ," can influence the development of obesity and related metabolic disorders. Diet is significantly important in shaping the structure and modulating the function of the gut microbiota. Apigenin (Api) widely exists in fruits and vegetables as a naturally occurring flavonoid and has anti-obesogenic, anti-inflammatory, and anti-carcinogenic properties. Its low bioavailability means it has enough time to interact with the intestine thus becomes a potential substrate for the gut intestine; thus, contributing to gut health. Here, we show that Api reduces whole-body weight, low-grade inflammation, and insulin resistance in high-fat diet (HFD)-induced obese mice. Our results reflect that Api supplementation can substantially improve intestinal dysbiosis triggered by HFD and restores gut barrier damage by alleviating metabolic endotoxemia. Augmentation of Akkermansia and Incertae_Sedis along with reduction of Faecalibaculum and Dubosiella at the genus level potentially mediated the protective effects of Api on metabolic syndrome. Furthermore, we show that the impact of Api on the reduction of body weight and the modification of gut microbiota could be transferred from Api-administered mice to HFD-feeding mice via horizontal fecal microbiota transplantation. Taken together, our data highlight the prebiotic role of Api and show its contribution to the restraint of gut dysbiosis and metabolic deterioration associated with obesity in mice.
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Although biological nitrogen (N) fixation (BNF) is an important N input process in subtropical forest ecosystems, how the diazotrophic communities related to this process respond to N and phosphorus (P) inputs is largely unknown. We investigated the effects of exogenous N and/or P inputs on N2-fixation activity, diazotrophic abundance and community composition using a continuous application of fertilizers over 5years experiment in a Chinese fir plantation. The fertilization regimes included control (CK), P treatment (P), low N addition treatment (N1), high N addition treatment (N2), low N and P addition treatment (N1P) and high N with P addition treatment (N2P). N2-fixation activity was determined using the acetylene reduction assay (ARA). Quantitative PCR and Illumina Miseq sequencing of nifH gene were performed to analyze diazotrophic abundance and community composition, respectively. Our results showed that P addition increased N2-fixation activity and nifH gene abundance by 189.07nmol C2H4 and 1.02×107copiesg-1 dry soil, respectively, while were reduced by 1.19nmol C2H4 and 2.04×106copiesg-1 dry soil when N was added. The application of P with low N (N1P) effectively alleviated the inhibitory effect of N input on N2-fixation activity. N-related treatments resulted in significant decreases in operational taxonomic unit (OTU) richness and shifts in diazotrophic community structure. N2-fixation activity and nifH gene abundance were strongly and positively correlated with soil pH and negatively correlated with mineral N (NH4+-N and NO3--N) contents, while mineral N concentrations rather than soil pH appeared to be the main factor altering diazotrophic community structure. These results revealed that P addition played a positive role in regulating biological nitrogen fixation in subtropical forest ecosystems.
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Cunninghamia/microbiologia , Fertilizantes , Fixação de Nitrogênio , Nitrogênio/análise , Fósforo/análise , Microbiologia do Solo , China , Florestas , Genes BacterianosRESUMO
The -889 C/T polymorphism in the interleukin-1α (IL-1α) gene has been implicated in the risk of cancer, but the results are inconclusive. The present meta-analysis aimed to investigate the association between the -889 C/T polymorphism and cancer risk. A literature search in PubMed, Embase™, Web of Science™, Science Direct(®), SpringerLink, EBSCO, Wanfang, and Chinese National Knowledge Infrastructure (CNKI) databases was carried out to identify studies investigating the association between IL-1α -889 C/T polymorphism and cancer risk. The odds ratio (OR) with 95% confidence interval (CI) were used to assess the strength of association. A total of 20 publications, involving 6,782 cases and 7,767 controls, were included in this meta-analysis. Combined analysis revealed a significant association between -889 C/T polymorphism and cancer risk under an allele model (OR =1.12, 95% CI =1.02-1.24, P=0.02), recessive model (OR =1.34, 95% CI =1.06-1.68, P=0.01), and homozygous comparison (OR =1.38, 95% CI =1.10-1.74, P<0.01). Subgroup analysis by ethnicity showed there was significant association between cancer risk and IL-1α -889C/T polymorphism in Asian populations under a recessive model (OR =2.57, 95% CI =1.11-5.98, P=0.03) and homozygous comparison (OR =2.60, 95% CI =1.12-6.04, P=0.03). Moreover, a subgroup analysis was conducted by source of control, and a statistically increased cancer risk was found in the hospital-based group, under a recessive model (OR =1.62, 95% CI =1.03-2.56, P=0.04) and homozygous comparison (OR =1.67, 95% CI =1.04-2.68, P=0.03). This meta-analysis suggests that IL-1α -889 C/T polymorphism contributes to cancer susceptibility. Further large and well-designed studies are needed to confirm this association.
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This study was aimed to compare the collection efficiency of mononuclear cells (MNC) from peripheral blood as well as the changes of blood-related indices in patient by using 3 cell separators. MNC were collected from 94 tumor patients by using Fenwal CS-3000plus, Haemonetics MCSplus and COBE spectra separators. Routine blood test was performed before and after MNC collection to detect the potential effects of cell separators on blood-related indices in the patients. MNC count was performed. The percentages of CD3(+), CD4(+) and CD8(+) in peripheral blood cells were determined. The results showed that the MNC counts were (3.08 ± 0.79)×10(9), (3.21 ± 1.12)×10(9), and (3.22 ± 1.84)×10(9) per bag by CS-3000plus, MCSplus and COBE spectra, respectively. And the corresponding decrease of platelet percentage was (6.86 ± 5.70)%, (8.05 ± 5.14)% and (5.89 ± 4.48)%, respectively. The CD3, CD4 and CD8 ratios in peripheral blood of patients before and after treatment were significantly statistical different (P < 0.001). It is concluded that the MNC collection can be performed successfully with CS-3000plus, MCSplus and COBE spectra, and their collections can meet the needs in clinic.
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Separação Celular/métodos , Células Matadoras Induzidas por Citocinas/citologia , Células Dendríticas/citologia , Leucaférese/instrumentação , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
OBJECTIVE: Human estrogen receptor α (ESR1), a member of the nuclear receptor superfamily of ligand-activated transcription factors, is one of the key mediators of hormonal response in estrogen-sensitive tissues. Accumulating evidence has demonstrated that two of the most widely studied single-nucleotide polymorphisms in ESR1 - PvuII (T/C, rs223493) and Xbal (A/G, rs9340799) - are possibly associated with Alzheimer's disease (AD). However, individual study results are still controversial. MATERIALS AND METHODS: We searched PubMed, Embase, Web of Science, Science Direct, SpringerLink, and the Chinese National Knowledge Infrastructure databases for eligible studies assessing the association of ESR1 polymorphisms and AD risk (last search performed in November 2013). Thereafter, a meta-analysis of 13,192 subjects from 18 individual studies was conducted to evaluate the association between ESR1 polymorphisms and susceptibility to AD. RESULTS: The results indicated that a significant association was found between the ESR1 PvuII polymorphism and AD risk in Caucasian populations (CC + CT versus TT, odds ratio [OR] 1.14, 95% confidence interval [CI] 1.02-1.28, P=0.03; CT versus TT, OR 1.16, 95% CI 1.02-1.31, P=0.02), whereas no evidence of association was found in Asian populations. Nevertheless, we did not find any significant association between the ESR1 XbaI polymorphism and AD risk for any model in Caucasian and Asian populations (all P>0.05). CONCLUSION: Based on this meta-analysis, we conclude that the ESR1 PvuII polymorphism might be a risk factor in AD development in Caucasian populations, not in Asian populations. Further confirmation is needed from better-designed and larger studies.
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Doença de Alzheimer/epidemiologia , Doença de Alzheimer/genética , Receptor alfa de Estrogênio/genética , Predisposição Genética para Doença/epidemiologia , Predisposição Genética para Doença/genética , Polimorfismo de Nucleotídeo Único , Idoso , Povo Asiático/genética , Povo Asiático/estatística & dados numéricos , Humanos , Fatores de Risco , População Branca/genética , População Branca/estatística & dados numéricosRESUMO
Recent studies have suggested that IL-18 -607C/A and -137G/C polymorphisms may be associated with the risk of allergic disease; however, individually published results are inconclusive. Therefore, we performed a meta-analysis to clarify whether IL-18 -607C/A and -137G/C polymorphisms were associated with the risk of allergic disease. A total of 21 studies including 5,331 cases and 9,658 controls were involved in this meta-analysis. In the overall analysis and the subgroup analysis according to ethnicity, we did not find significant association between IL-18 -607C/A or -137G/C polymorphism and the risk of allergic disease (all P > 0.05). However, in a stratified analysis by type of allergic disease, our results indicated that IL-18 -607C/A polymorphism was associated with a significantly decreased risk of allergic asthma in heterozygous comparison and IL-18 -137G/C was associated with a significantly decreased risk of allergic dermatitis in recessive model and homozygous comparison. In the stratified analysis by source of control, IL-18-607C/A showed significantly reduced risk in population-based subgroup, and for IL-18 -137G/C only significantly decreased risk was found in the hospital-based subgroup. Our meta-analysis suggests that IL-18 -607C/A and -137G/C polymorphisms may be protective factors for the risk of allergic asthma and allergic dermatitis, respectively.
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Asma/genética , Dermatite/genética , Hipersensibilidade/genética , Interleucina-18/genética , Asma/patologia , Dermatite/patologia , Estudos de Associação Genética , Predisposição Genética para Doença , Humanos , Hipersensibilidade/patologia , Polimorfismo de Nucleotídeo Único , Fatores de RiscoRESUMO
BACKGROUND: Genetic factors have been shown to play an important role in the development of cancers. However, individual studies may fail to completely demonstrate complicated genetic relationships because of small sample size. Therefore, we performed a meta-analysis to evaluate the association of E-selectin Ser128Arg (S128R) with cancer risk. MATERIALS AND METHODS: A literature search in PubMed, Embase, Web of Science, Science Direct, SpringerLink, EBSCO, Wanfang, and Chinese National Knowledge Infrastructure databases was carried out to identify studies of the association between E-selectin S128R polymorphism and cancer risk. The odds ratio (OR) with 95% confidence intervals (95%CIs) were used to assess the strength of association. RESULTS: A total of eight studies involving 1,675 cancer cases and 2,285 controls were included in the meta-analysis. In overall populations, S128R polymorphism seemed to be associated with cancer risk (Arg allele vs Ser allele: OR=1.65, 95%CI =1.33-2.04, p<0.01; Arg/Arg+Arg/Ser vs Ser/Ser: OR=1.87, 95%CI =1.48-2.36, p<0.01; Arg/Ser vs Ser/Ser: OR=1.80, 95%CI =1.51-2.14, p<0.01). Similarly, subgroup analysis by ethnicity and source of control also revealed that this polymorphism was related to cancer risk. CONCLUSIONS: Our meta-analysis revealed that there was association between the E-selectin S128R polymorphism and the risk of cancer. Further large and well-designed studies are needed to confirm this association.
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Carcinogênese/genética , Selectina E/genética , Neoplasias/genética , Predisposição Genética para Doença , Humanos , Neoplasias/epidemiologia , Polimorfismo de Nucleotídeo Único , Fatores de RiscoRESUMO
Toll-like receptors (TLRs) are well known as molecular sensors of pathogen-associated molecular patterns. They control activation of the innate immune response and subsequently shape the adaptive immune response. Polymorphisms in TLR3 gene associated with cancer have been studied extensively. However, the results remain controversial. A literature search was performed among PubMed, Embase, Web of Science, Science Direct, Wanfang, and Chinese National Knowledge Infrastructure databases to identify eligible studies on the association between TLR3 polymorphisms and cancer risk. A total of 12 studies in 11 articles were included in the meta-analysis including 5,861 cases and 6,339 controls. Significant associations with cancer risk were observed for single nucleotide polymorphisms (SNPs) rs3775291 (allele model: odds ratio (OR) = 1.12, 95 % confidence interval (95 % CI) = 1.00-1.25, P = 0.04), rs3775290 (allele model: OR = 1.12, 95 % CI = 1.00-1.25, P = 0.04; dominant model: OR = 1.30, 95 % CI = 1.05-1.60, P = 0.01; homozygous comparison: OR = 1.68, 95 % CI = 1.06-2.68, P = 0.03; heterozygous comparison: OR = 1.25, 95 % CI = 1.01-1.55, P = 0.04), rs5743305 (allele model: OR = 1.07, 95 % CI = 1.01-1.15, P = 0.03; dominant model: OR = 1.11, 95 % CI = 1.01-1.22, P = 0.03), and rs5743312 (allele model: OR = 1.13, 95 % CI = 1.01-1.27, P = 0.03; recessive model: OR = 1.86, 95 % CI = 1.31-2.63, P < 0.01; homozygous comparison: OR = 1.88, 95 % CI = 1.33-2.67, P < 0.01), respectively. Meanwhile, we did not find any significant association with cancer risk for rs7657186 and rs7668666. In conclusion, this meta-analysis indicates a significant association of four TLR3 gene polymorphisms with cancer risk. However, because the study size was limited, further studies are essential to confirm our results.
Assuntos
Predisposição Genética para Doença , Neoplasias/genética , Polimorfismo de Nucleotídeo Único , Receptor 3 Toll-Like/genética , Humanos , Neoplasias/etiologia , Viés de Publicação , RiscoRESUMO
BACKGROUND: Emerging evidence showed that VEGF gene polymorphisms are involved in the regulation of VEGF protein expression, thus increasing an individual's susceptibility to preeclampsia (PE); but individually published results are inconclusive. The aim of this meta-analysis was to investigate the associations between VEGF gene polymorphisms and PE risk. METHODS: A systematic literature search of MEDLINE, Embase, Web of Science, and CNKI (Chinese National Knowledge Infrastructure) databases was conducted. Statistical analyses were performed using STATA 12.0 software and Review manager 5.1. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. RESULTS: According to the inclusion criteria, 11 case-control studies were finally included in this meta-analysis. A total of 1,069 PE cases and 1,315 controls were included in this study. Our meta-analysis indicated that VEGF +936C/T (T vs. C, ORâ=â1.52, 95%CIâ=â1.08-2.12) or -634G/C polymorphism (C vs. G, ORâ=â1.24, 95% CIâ=â1.03-1.50) was associated with the risk of PE, whereas there was no association between -2578C/A (A vs. C, ORâ=â0.98, 95%CIâ=â0.82-1.16) or -1154G/A (A vs. G, ORâ=â1.30, 95%CIâ=â0.94-1.78) polymorphism and PE risk in our study. CONCLUSION: Our meta-analysis suggested that VEGF -2578C/A or -1154G/A polymorphism had no association with PE risk in all examined patients, whereas there was an association between VEGF +936C/T or -634G/C polymorphism and risk of PE.