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1.
J Plant Biol ; : 1-14, 2021 Jan 04.
Artigo em Inglês | MEDLINE | ID: mdl-33424241

RESUMO

Although morphology and grain size are important to rice growth and yield, the identity of abundant natural allelic variations that determine agronomically important differences in crops is unknown. Here, we characterized the function of mitogen-activated protein kinase 3 from Oryza officinalis Wall. ex Watt encoded by OrMKK3. Different alternative splicing variants occurred in OrMKK3. Green fluorescent protein (GFP)-OrMKK3 fusion proteins localized to the cell membrane and nuclei of rice protoplasts. Overexpression of OrMKK3 influenced the expression levels of the grain size-related genes SMG1, GW8, GL3, GW2, and DEP3. Phylogenetic analysis showed that OrMKK3 is well conserved in plants while showing large amounts of variation between indica, japonica, and wild rice. In addition, OrMKK3 slightly influenced brassinosteroid (BR) responses and the expression levels of BR-related genes. Our findings thus identify a new gene, OrMKK3, influencing morphology and grain size and that represents a possible link between mitogen-activated protein kinase and BR response pathways in grain growth. Supplementary Information: The online version contains supplementary material available at 10.1007/s12374-020-09290-2.

2.
Physiol Mol Biol Plants ; 26(11): 2173-2187, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-33268921

RESUMO

Self-germinated seedlings of Citrus sinensis and C. grandis were supplied with nutrient solution with 0 mM AlCl3·6H2O (control, -Al) or 1 mM AlCl3·6H2O (+Al) for 18 weeks. The DW (Dry weights) of leaf, stem, shoot and the whole plant of C. grandis were decreased and the ratio of root DW to shoot DW in C. grandis were increased by Al, whereas these parameters of C. sinensis were not changed by Al. Al treatment dramatically decreased the sulfur (S) content in C. grandis roots and the phosphorus (P) content in both C. sinensis and C. grandis roots. More Al was transported to shoots and leaves in C. grandis than in C. sinensis under Al treatment. Al treatment has more adverse effects on C. grandis than on C. sinensis, as revealed by the higher production of superoxide anion (O2 ·-), H2O2 and thiobarbituric acid reactive substace (TBARS) content in C. grandis roots. Via the Illumina sequencing technique, we successfully identified and quantified 12 and 16 differentially expressed miRNAs responding to Al stress in C. sinensis and C. grandis roots, respectively. The possible mechanism underlying different Al tolerance of C. sinensis and C. grandis were summarized as having following aspects: (a) enhancement of adventitious and lateral root development (miR160); (b) up-regulation of stress and signaling transduction related genes, such as SGT1, PLC and AAO (miR477, miR397 and miR398); (c) enhancement of citrate secretion (miR3627); (d) more flexible control of alternative glycolysis pathway and TCA cycle (miR3627 and miR482); (e) up-regulation of S-metabolism (miR172); (f) more flexible control of miRNA metabolism. For the first time, we showed that root development (miR160) and cell wall components (cas-miR5139, csi-miR12105) may play crucial roles in Al tolerance in citrus plants. In conclusion, our study provided a comprehensive profile of differentially expressed miRNAs in response to Al stress between two citrus plants differing in Al tolerance which further enriched our understanding of the molecular mechanism underlying Al tolerance in plants.

3.
PLoS Negl Trop Dis ; 14(10): e0008801, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-33119592

RESUMO

Severe Fever with Thrombocytopenia Syndrome (SFTS) is an emerging infectious disease caused by a novel bunyavirus, SFTS virus (SFTSV), with fatal outcome developed in approximately 17% of the cases. Thrombocytopenia is a hallmark feature of SFTS, and associated with a higher risk of fatal outcome, however, the pathophysiological involvement of platelet in the clinical outcome of SFTS remained under-investigated. In the current study, by retrospectively analyzing 1538 confirmed SFTS patients, we observed that thrombocytopenia was associated with enhanced activation of the cytokine network and the vascular endothelium, also with a disturbed coagulation response. The platelet phenotypes were also extensively altered in the process of thrombocytopenia development of SFTS patients. More importantly, all these disturbed host responses were related to the severity of thrombocytopenia, thus were considered to play in a synergistic way to influence the disease outcome. Moreover, the clinical effect of platelet transfusion was assessed by comparing two groups of patients with or without receiving this therapy. As a result, we observed no therapy effect in altering frequencies of fatal outcome, clinical bleeding development, or dynamic change of platelet count during the hospitalization. It's suggested that platelet supplementation alone acted a minor role in improving disease outcome, therefore new therapeutic intervention to regulate host response should be proposed. The current results revealed some evidence of interrelationship between platelet count and clinical outcome of SFTS disease from the perspective of activation of the cytokine network, the vascular endothelium, and the coagulation/fibrinolysis system. These evaluations might help to attain a better understanding of the pathogenesis and therapy choice in SFTS.

4.
World J Emerg Med ; 11(4): 216-222, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33014217

RESUMO

BACKGROUND: Fluid management is crucial to acute respiratory distress syndrome (ARDS) secondary to sepsis. However, choices of fluid resuscitation strategies and fluid input volumes remain a thorny problem. Our study aimed to elucidate the relationship between fluid balance and prognosis of ARDS patients secondary to sepsis. METHODS: Our study included 322 sepsis patients from Ruijin Hospital between 2014 and 2018, and 84 patients were diagnosed as ARDS within 72 hours after onset of sepsis according to Berlin ARDS Definition. RESULTS: Among the 322 sepsis patients, 84 (26.1%) were complicated with ARDS within 72 hours. ARDS patients had a lower oxygenation index (PaO2/FiO2 166.4±71.0 vs. 255.0±91.2, P<0.05), longer duration of mechanical ventilation (11 [6-24] days vs. 0 [0-0] days, P<0.05) than those without ARDS. Sepsis patients with ARDS showed daily positive net fluid balance during seven days compared with those without ARDS who showed daily negative net fluid balance since the second day with significant statistical differences. Among the 84 sepsis patients with ARDS, 58 (69.0%) died. Mean daily fluid input volumes were much lower in survivors than in non-survivors (43.2±16.7 mL/kg vs. 51.0±25.2 mL/kg, P<0.05) while output volumes were much higher in survivors (45.2±19.8 mL/kg vs. 40.2±22.7 mL/kg, P<0.05). Using binary logistic regression analysis, we found that the mean daily fluid balance was independently associated with mortality of sepsis patients complicating with ARDS (P<0.05). CONCLUSIONS: Early negative fluid balance is independently associated with a better prognosis of sepsis patients complicated with ARDS.

5.
J Infect ; 81(5): 776-784, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32956725

RESUMO

Human immunodeficiency virus (HIV) infection impairs both cellular and humoral immune system. Follicular regulatory T (Tfr) cells are a recently characterised subset of CD4+T cells. Tfr also exerts an immunosuppressive effect on humoral immune system through interaction with follicular helper T (Tfh) cells, but the role of Tfr in HIV infection needs to be further elucidated. 20 treatment-naïve and 20 antiretroviral therapy (ART)-treated HIV-infected individuals were enrolled for cross-sectional study and nine complete responders (CRs) and eight immune non-responders (INRs) after ART were collected for retrospective cohort study. Tfr phenotypes, cytokine secretions, and apoptosis of those subjects were evaluated by flow cytometry. HIV DNA was measured by reverse transcription-quantitative PCR (RT-qPCR). Significantly increased circulating Tfr was observed in chronic HIV+ patients and the imbalance between Tfr and Tfh17 was associated with CD4+T counts. In addition, an elevated proportion of Tfr was associated with immune reconstruction failure of patients after ART. The IL-10 and CTLA-4 expressions of Tfr cells were up-regulated in treatment-naïve HIV+ patients. Ex vivo experiments showed IL-10 and CTLA-4 expressed by Tfr inhibited IL-21 secretion of Tfh. Tfr harboured a comparable HIV-1 DNA level with Tfh in HIV+ patients. Compared to Tfr of HCs, Tfr cells of HIV+ patients were more insensitive to CD95 and IFN-α induced apoptosis, had a higher proliferation rate, and had more stem-like T cell (Tscm) phenotype. The anti-apoptosis feature, higher proliferation rate, and Tscm-like features of Tfr in HIV+ patients, led to the expansion of Tfr which in turn resulted in dysfunction of Tfh. Tfr cells were also involved in immune reconstruction failure and latent infection of HIV. Tfr cells were a novel, and potentially therapeutic, target for the cure of HIV infection, especially for HIV vaccine development and HIV reservoir elimination.

7.
World J Clin Cases ; 8(14): 2942-2949, 2020 Jul 26.
Artigo em Inglês | MEDLINE | ID: mdl-32775376

RESUMO

BACKGROUND: Lumbar disc herniation is a common disease. Endoscopic treatment may have more advantages than traditional surgery. AIM: To compare the clinical efficacy and safety of microendoscopic discectomy (MED) and open discectomy with lamina nucleus enucleation in the treatment of single-segment lumbar intervertebral disc herniation. METHODS: Ninety-six patients who were operated at our hospital were selected for this study. Patients with single-segment lumbar disc herniation were admitted to the hospital from March 2018 to March 2019 and were randomly divided into the observation group and the control group with 48 cases in each group. The former group underwent lumbar discectomy and the latter underwent laparotomy and nucleus pulpectomy. Surgical effects were compared between the two groups. RESULTS: In terms of surgical indicators, the observation group had a longer operation time, shorter postoperative bedtime and hospital stay, less intraoperative blood loss, and smaller incision length than the control group (P < 0.05). The excellent recovery rate did not differ significantly between the observation group (93.75%) and the control group (91.67%). Visual analogue scale pain scores were significantly lower in the observation group than in the control group at 1 d, 3 d, 1 mo, and 6 mo after surgery (P < 0.05). The incidence of complications was significantly lower in the observation group than in the control group (6.25% vs 22.92%, P < 0.05). CONCLUSION: Both MED and open discectomy can effectively improve single-segment lumbar disc herniation, but MED is associated with less trauma, less bleeding, and a lower incidence of complications.

8.
World J Gastroenterol ; 26(19): 2349-2373, 2020 May 21.
Artigo em Inglês | MEDLINE | ID: mdl-32476798

RESUMO

BACKGROUND: Pancreatic cancer (PC) is one of the deadliest cancers worldwide. PC metastasis involves a complex set of events, including epithelial-mesenchymal transition (EMT), that increase tumor cell invasiveness. Recent evidence has shown that hypoxia is a major EMT regulator in pancreatic cancer cells and facilitates metastasis; however, the mechanisms remain elusive. AIM: To investigate the role of miR-301a in hypoxia-induced EMT in PC cells. METHODS: Real-time PCR and Western blot analysis were used to detect the expression of miR-301a and EMT markers in PDAC cells cultured in hypoxic and normoxic conditions. Western blot analysis was used to detect the expression of EMT markers in PDAC cells with miR-301a overexpression. Wound healing assay and Transwell assay were used to detect the migration capabilities of PDAC cells with miR-301a overexpression and knockout. Luciferase assay was used to detect the miR-301a promoter and the 3' untranslated region activity of TP63. Orthotopic PC mouse models were used to study the role of miR-301a in metastasis of PDAC cells in vivo. In situ hybridization assay was used to detect the expression of miR-301a in PDAC patient samples (adjacent paratumor and paired tumor tissues). . RESULTS: Hypoxic environment could directly promote the EMT of PC cells. The expression level of miR-301a was increased in a HIF2α dependent manner in hypoxia-cultured CFPAC-1 and BxPC-3 cells. Overexpression of miR-301a enhanced the hypoxia-induced EMT of PC cells, while knocking out miR-301a result in the suppression of hypoxia-induced EMT. TP63 was a direct target of miR-301a and involved in the metastatic process of PC cells. Furthermore, miR-301a upregulation facilitated PDAC distant metastasis and lymph node metastasis in vivo. Additionally, miR-301a overexpression was indicative of aggressive clinicopathological behaviors and poor prognosis. CONCLUSION: The newly identified HIF-2α-miR301a-TP63 signaling pathway may play a crucial role in hypoxia-induced EMT in PDAC cells.

9.
J Clin Lipidol ; 14(4): 498-506, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32561169

RESUMO

BACKGROUND: The etiology of hypertriglyceridemia (HTG) and, consequently, HTG-induced acute pancreatitis (HTG-AP), is complex. OBJECTIVE: Herein, we explore a possible gene-environment interaction between APOA5 c.553G>T (p.185Gly>Cys, rs2075291), a common variant associated with altered triglyceride levels, and pregnancy in HTG-AP. METHODS: We enrolled 318 Chinese HTG-AP patients and divided them into 3 distinct groups: Group 1, male patients (n = 183); Group 2, female patients whose disease was unrelated to pregnancy (n = 105); and Group 3, female patients whose disease was related to pregnancy (n = 30). APOA5 rs2075291 genotype status was determined by Sanger sequencing. A total of 362 healthy Han Chinese subjects were used as controls. Data on body mass index, peak triglyceride level, age of disease onset, episode number, and clinical severity of HTG-AP were collected from each patient. Multiple comparisons, between patient groups, between patient groups and controls, or within each patient group, were performed. RESULTS: A robust association of APOA5 rs2075291 with HTG-AP in general, and HTG-AP during pregnancy in particular, was demonstrated. The minor T allele showed a stronger association with Group 3 patients than with either Group 1 or Group 2 patients. This stronger association was due mainly to the much higher frequency of TT genotype in Group 3 patients (20%) than that (<6%) in Group 1 and Group 2 patients. Moreover, the TT genotype was associated with a significantly higher peak triglyceride level in Group 3 patients compared with the GG genotype. CONCLUSION: Our findings provide evidence for an interaction between APOA5 rs2075291 and pregnancy in HTG-AP.

10.
Lipids Health Dis ; 19(1): 63, 2020 Apr 07.
Artigo em Inglês | MEDLINE | ID: mdl-32264896

RESUMO

BACKGROUND: Hypertriglyceridemia (HTG) is a leading cause of acute pancreatitis. HTG can be caused by either primary (genetic) or secondary etiological factors, and there is increasing appreciation of the interplay between the two kinds of factors in causing severe HTG. OBJECTIVES: The main aim of this study was to identify the genetic basis of hypertriglyceridemia-induced acute pancreatitis (HTG-AP) in a Chinese family with three affected members (the proband, his mother and older sister). METHODS: The entire coding and flanking sequences of LPL, APOC2, APOA5, GPIHBP1 and LMF1 genes were analyzed by Sanger sequencing. The newly identified LPL nonsense variant was subjected to functional analysis by means of transfection into HEK-293 T cells followed by Western blot and activity assays. Previously reported pathogenic LPL nonsense variants were collated and compared with respect to genotype and phenotype relationship. RESULTS: We identified a novel nonsense variant, p.Gln118* (c.351C > T), in the LPL gene, which co-segregated with HTG-AP in the Chinese family. We provided in vitro evidence that this variant resulted in a complete functional loss of the affected LPL allele. We highlighted a role of alcohol abuse in modifying the clinical expression of the disease in the proband. Additionally, our survey of 12 previously reported pathogenic LPL nonsense variants (in 20 carriers) revealed that neither serum triglyceride levels nor occurrence of HTG-AP was distinguishable among the three carrier groups, namely, simple homozygotes, compound heterozygotes and simple heterozygotes. CONCLUSIONS: Our findings, taken together, generated new insights into the complex etiology and expression of HTG-AP.

11.
Nat Plants ; 6(4): 416-426, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-32284549

RESUMO

The circadian clock is synchronized by environmental cues, mostly by light and temperature. Explaining how the plant circadian clock responds to temperature oscillations is crucial to understanding plant responsiveness to the environment. Here, we found a prevalent temperature-dependent function of the Arabidopsis clock component EARLY FLOWERING 4 (ELF4) in the root clock. Although the clocks in roots are able to run in the absence of shoots, micrografting assays and mathematical analyses show that ELF4 moves from shoots to regulate rhythms in roots. ELF4 movement does not convey photoperiodic information, but trafficking is essential for controlling the period of the root clock in a temperature-dependent manner. Low temperatures favour ELF4 mobility, resulting in a slow-paced root clock, whereas high temperatures decrease movement, leading to a faster clock. Hence, the mobile ELF4 delivers temperature information and establishes a shoot-to-root dialogue that sets the pace of the clock in roots.

13.
Mol Genet Genomic Med ; 8(3): e1048, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31962008

RESUMO

BACKGROUND: Acute pancreatitis in pregnancy (APIP) is a life-threatening disease for both mother and fetus. To date, only three patients with recurrent hypertriglyceridemia-induced APIP (HTG-APIP) have been reported to carry rare variants in the lipoprotein lipase (LPL) gene, which encodes the key enzyme responsible for triglyceride (TG) metabolism. Coincidently, all three patients harbored LPL variants on both alleles and presented with complete or severe LPL deficiency. METHODS: The entire coding regions and splice junctions of LPL and four other TG metabolism genes (APOC2, APOA5, GPIHBP1, and LMF1) were analyzed by Sanger sequencing in a Han Chinese patient who had experienced two episodes of HTG-APIP. The impact of a novel LPL missense variant on LPL protein expression and activity was analyzed by transient expression in HEK293T cells. RESULTS: A novel heterozygous LPL missense variant, p.His210Leu (c.629A > T), was identified in our patient. This variant did not affect protein synthesis but significantly impaired LPL secretion and completely abolished the enzymatic activity of the mutant protein. CONCLUSION: This report describes the first identification and functional characterization of a heterozygous variant in the LPL that predisposed to recurrent HTG-APIP. Our findings confirm a major genetic contribution to the etiology of individual predisposition to HTG-APIP.

14.
J Gastroenterol Hepatol ; 35(4): 689-695, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31519041

RESUMO

BACKGROUND AND AIM: Hepatitis B-associated liver cirrhosis (HBC) leads to profound alterations of immune systems, especially disruptions of B cell immune responses. CXCR5+ CD4+ T cells (including T follicular helper [Tfh] cells and T follicular regulatory [Tfr] cells) are responsible for the regulation of B cell functions. The aim of this study was to dissect the roles of CXCR5+ CD4+ T cell subset in B cell disruption caused by HBC. METHODS: Forty-one patients with HBC and 15 healthy controls were enrolled in this study. ELISA, flow cytometric analysis, and cell coculture were performed to analyze the properties of Tfh and Tfr. RESULTS: We observed significantly decreased memory B cells and increased plasma B cells in HBC patients, as well as significant upregulation of lipopolysaccharide binding protein and soluble CD14 in plasma of decompensated HBCs patients. The downregulation of Tfh17 was observed in HBC patients with spontaneous bacterial peritonitis compared with those without. The decrease of Tfh17 was paralleled with Child-Pugh grade and negatively correlated with plasma B cells and soluble CD14 in HBC patients. Interleukin (IL)-21+ Tfh of HBC patients was also downregulated compared with healthy controls, and it was positively correlated with memory B cells and the upregulation of IL-10+ Tfr. It was then revealed that Tfr could inhibit the secretion of IL-21 by Tfh, and the blocking of IL-10 could diminish this effect. CONCLUSIONS: The changes of the frequency and function of Tfh and Tfr may play an important role in disease progression and immune dysfunction of HBC.


Assuntos
Antígenos CD4 , Hepatite B/complicações , Hepatite B/imunologia , Cirrose Hepática/etiologia , Cirrose Hepática/imunologia , Receptores CXCR5 , Linfócitos T Auxiliares-Indutores/imunologia , Linfócitos T Reguladores/imunologia , Adulto , Linfócitos B/imunologia , Feminino , Humanos , Interleucina-10 , Interleucinas , Receptores de Lipopolissacarídeos/sangue , Masculino , Pessoa de Meia-Idade
15.
New Phytol ; 225(4): 1732-1745, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31608986

RESUMO

The mechanisms involved in the regulation of gene expression in response to phosphate (Pi) deficiency have been extensively studied, but their chromatin-level regulation remains poorly understood. We examined the role of histone acetylation in response to Pi deficiency by using the histone deacetylase complex1 (hdc1) mutant. Genes involved in root system architecture (RSA) remodeling were analyzed by quantitative real-time polymerase chain reaction (qPCR) and chromatin immunoprecipitation qPCR. We demonstrate that histone H3 acetylation increased under Pi deficiency, and the hdc1 mutant was hypersensitive to Pi deficiency, with primary root growth inhibition and increases in root hair number. Concomitantly, Pi deficiency repressed HDC1 protein abundances. Under Pi deficiency, hdc1 accumulated higher concentrations of Fe3+ in the root tips and had higher expression of genes involved in RSA remodeling, such as ALUMINUM-ACTIVATED MALATE TRANSPORTER1 (ALMT1), LOW PHOSPHATE ROOT1 (LPR1), and LPR2 compared with wild-type plants. Furthermore, Pi deficiency enriched the histone H3 acetylation of ALMT1 and LPR1. Finally, genetic evidence showed that LPR1/2 was epistatic to HDC1 in regulating RSA remodeling. Our results suggest a chromatin-level control of Pi starvation responses in which HDC1-mediated histone H3 deacetylation represses the transcriptional activation of genes involved in RSA remodeling in Arabidopsis.

16.
Plant Cell Environ ; 43(2): 463-478, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31713247

RESUMO

Transcriptional regulation is important for plants to respond to toxic effects of aluminium (Al). However, our current knowledge to these events is confined to a few transcription factors. Here, we functionally characterized a rice bean (Vigna umbellata) NAC-type transcription factor, VuNAR1, in terms of Al stress response. We demonstrated that rice bean VuNAR1 is a nuclear-localized transcriptional activator, whose expression was specifically upregulated by Al in roots but not in shoot. VuNAR1 overexpressing Arabidopsis plants exhibit improved Al resistance via Al exclusion. However, VuNAR1-mediated Al exclusion is independent of the function of known Al-resistant genes. Comparative transcriptomic analysis revealed that VuNAR1 specifically regulates the expression of genes associated with protein phosphorylation and cell wall modification in Arabidopsis. Transient expression assay demonstrated the direct transcriptional activation of cell wall-associated receptor kinase 1 (WAK1) by VuNAR1. Moreover, yeast one-hybrid assays and MEME motif searches identified a new VuNAR1-specific binding motif in the promoter of WAK1. Compared with wild-type Arabidopsis plants, VuNAR1 overexpressing plants have higher WAK1 expression and less pectin content. Taken together, our results suggest that VuNAR1 regulates Al resistance by regulating cell wall pectin metabolism via directly binding to the promoter of WAK1 and induce its expression.

17.
Drug Des Devel Ther ; 13: 3391-3404, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31576113

RESUMO

Purpose: It has been reported that approximately 40% of ALI (acute lung injury) incidence resulted from sepsis. Paclitaxel, as a classic anti-cancer drug, plays an important role in the regulation of inflammation. However, we do not know whether it has a protective effect against CLP (cecal ligation and puncture)-induced septic ALI. Our study aims to illuminate the mitigative effects of paclitaxel on sepsis-induced ALI and its relevant mechanisms. Materials and methods: The survival rates and organ injuries were used to evaluate the effects of paclitaxel on CLP mice. The levels of inflammatory cytokines were tested by ELISA. MUC1 siRNA pre-treatment was used to knockdown MUC1 expression in vitro. GO203 was used to inhibit the homodimerization of MUC1-C in vivo. The expression levels of MUC1, TLR 4 and p-NF-κB/p65 were detected by Western blot. Results: Our results showed that paclitaxel improved the survival rates and ameliorated organ injuries especially lung injury in CLP-induced septic mice. These were accompanied by reduced inflammatory cytokines in sera and BALF (bronchoalveolar lavage fluid). We also found paclitaxel could attenuate TLR 4-NF-κB/p65 activation both in lung tissues of septic mice and LPS-stimulated lung type II epithelial cell line A549. At the upstream level, paclitaxel-upregulated expression levels of MUC1 in both in vivo and in vitro experiments. The inhibitory effects of paclitaxel on TLR 4-NF-κB/p65 activation were reversed in lung tissues of septic mice pre-treated with MUC1 inhibitor and in MUC1-knockdown A549 cells. Protection of paclitaxel on sepsis-induced ALI and decrease of inflammatory cytokines were also abolished by inhibition of MUC1. Conclusion: Collectively, these results indicated paclitaxel could significantly alleviate acute lung injury in CLP-induced septic mice and LPS-stimulated lung type II epithelial cell line A549 by activating MUC1 and suppressing TLR-4/NF-κB pathway.


Assuntos
Lesão Pulmonar Aguda/tratamento farmacológico , Anti-Inflamatórios/farmacologia , Mucina-1/metabolismo , NF-kappa B/antagonistas & inibidores , Paclitaxel/farmacologia , Sepse/tratamento farmacológico , Receptor 4 Toll-Like/antagonistas & inibidores , Lesão Pulmonar Aguda/metabolismo , Animais , Anti-Inflamatórios/administração & dosagem , Ceco/cirurgia , Injeções Intraperitoneais , Masculino , Camundongos , Camundongos Endogâmicos C57BL , NF-kappa B/metabolismo , Paclitaxel/administração & dosagem , Punções/efeitos adversos , Sepse/metabolismo , Receptor 4 Toll-Like/metabolismo
19.
Genet Test Mol Biomarkers ; 23(7): 442-447, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31219360

RESUMO

Background: Single nucleotide polymorphisms (SNPs) within precursor microRNAs (miRNAs) can affect the expression of the miRNAs and may be involved in the pathogenesis of pulmonary tuberculosis (PTB) and extrapulmonary tuberculosis (EPTB). Aims: We investigated the potential associations among four precursor miRNA SNPs (miR-149 A>G, C>T; miR-196a2 C>T; miR-499 C>T) and both PTB and EPTB. Methods: The study included 380 PTB patients, 242 EPTB patients, and 606 healthy control (HC) subjects from a Chinese Han population. We determined the miRNA relative expression levels from 10 HCs and 10 tuberculosis (TB) patients by quantitative PCR. Results: We found that the PTB group had a significantly lower miR-149 level (p < 0.05) versus the HCs. The allele and genotype frequencies of the miR-149 SNPs were significantly different between the TB patients and the HC group. The C allele at the rs2292832 and the A allele at the rs71428439 locus were associated with susceptibility to EPTB. The C allele of rs2292832 was associated with an increased risk of EPTB compared with that of HCs (p < 0.01), and the A allele of rs71428439 was protective against EPTB (p < 0.01) and PTB (p < 0.01). Conclusions: We identified genetic polymorphisms in miR-149 that appear to be associated with susceptibility to both PTB and EPTB within a Chinese population.


Assuntos
MicroRNAs/genética , Polimorfismo de Nucleotídeo Único , Tuberculose Pulmonar/genética , Tuberculose/genética , Adulto , Alelos , China , Feminino , Expressão Gênica , Estudos de Associação Genética , Predisposição Genética para Doença , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Precursores de RNA
20.
Zhongguo Dang Dai Er Ke Za Zhi ; 21(4): 381-386, 2019 Apr.
Artigo em Chinês | MEDLINE | ID: mdl-31014433

RESUMO

OBJECTIVE: To study the etiology and genetic diagnosis of children with short stature. METHODS: A retrospective analysis was performed to study the etiological distribution and clinical features of 86 children with short stature. RESULTS: A total of 6 causes were observed in these children, among which idiopathic short stature (ISS, 41%) and growth hormone deficiency (GHD, 29%) were the most common causes, followed by genetic diseases (14%). There were no significant differences in age at the time of diagnosis, body height, body length and weight at birth, body height of parents and insulin-like growth factor-1 levels between the genetic disease group and the ISS/GHD groups (P>0.05). Compared with the ISS group, the genetic disease group had significantly lower deviation from the 3rd percentile for the height of children of the same age and sex (ΔP3) and height standard deviation score (P<0.05), while there were no significant differences between the genetic disease and GHD groups (P>0.05). The analysis of the clinical manifestations for the genetic disease group showed heterogeneity and phenotypic overlap in children with different genetic diseases. CONCLUSIONS: ISS, GHD and genetic diseases are major causes of short stature in children. For children with severe short stature, genetic testing should be performed to make a definitive diagnosis after GHD has been excluded.


Assuntos
Testes Genéticos , Estatura , Criança , Nanismo Hipofisário , Transtornos do Crescimento , Hormônio do Crescimento Humano , Humanos , Estudos Retrospectivos
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