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1.
Biol Trace Elem Res ; 2020 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-32002792

RESUMO

Iron overload is harmful to health and associates with intracellular excessive reactive oxygen species (ROS) generation. Nobiletin (Nob) is known to be antioxidant and anti-inflammatory. However, whether Nob can protect endothelial cells against iron overload has not been studied, and the specific mechanism has not yet been elucidated. In this study, we have identified the protective effects of Nob, and its underlying molecular mechanism in human umbilical vein endothelial cells (HUVECs) suffered from iron overload via ROS/ADMA/DDAHII/eNOS/NO pathway. We found that compared with 50 µM iron dextran treatment, co-treatment with 20 µM Nob increased cell viability and decreased lactate dehydrogenase activity. Besides, Nob could upregulate DDAHII expression and activity, promote eNOS phosphorylation to produce more NO, reduce ADMA content, and therefore increase superoxide dismutase, catalase, and glutathione peroxidase activities, and decrease malondialdehyde level and ROS generation. Nob also inhibited mitochondrial permeability transition pore (mPTP) openness and cleaved caspase-3 expression, and decreased apoptosis induced by iron overload. These results were consistent when Nob was replaced by the positive control reagents L-arginine (a competitive substrate of ADMA), cyclosporin A (an mPTP closing agent), or edaravone (a free radical scavenger). The addition of pAD/DDAHII-shRNA adenovirus reversed the above effects of Nob. These data suggested that the protective mechanism of Nob was to inhibit ROS burst, upregulate DDAHII expression and activity, promote eNOS phosphorylation, produce NO, reduce ADMA content, and ultimately alleviate iron overload damage in vascular endothelium.

2.
Enzyme Microb Technol ; 134: 109485, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32044032

RESUMO

Increasing the metabolic flux of the mevalonate pathway, reducing the metabolic flux of competing pathway and utilizing the diauxie-inducible system constructed by GAL promoters are strategies commonly used in yeast metabolic engineering for the production of terpenoids. Using these strategies, we constructed a series of yeast strains with a strengthened mevalonate pathway and finally produced 336.5 mg/L nerolidol in a shake flask. The spliced HAC1 mRNA assay indicated that the unfolded protein response (UPR) occurred in the strains that we constructed. UPR strains exhibited the low transcriptional activities of GAL1 promoter. HAC1-overexpressing strain exhibited dramatically enhanced transcriptional activity of GAL1 promoter at 72 h of fermentation in flasks. HAC1 overexpression also increased the nerolidol titer by 47.7 %, reaching 497.0 mg/L and increased cell vitality. RNA-seq showed that the genes whose transcription responded to HAC1-overexpression were involved in the regulation of monocarboxylic acid metabolic processes and cellular amino acid biosynthetic process, indicating that the metabolic regulation may be part of the reason of the improved nerolidol synthesis. Our findings enrich the knowledge of the relationship between the construction of sesquiterpene-producing cell factories and UPR regulation. This study provides an effective strategy for sesquiterpene production in yeast.

3.
Mol Cancer ; 19(1): 17, 2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-31992303

RESUMO

BACKGROUND: Recent evidences have shown that circular RNAs (circRNAs) are frequently dysregulated and play paramount roles in various cancers. circRNAs are abundant in central nervous system (CNS); however, few studies describe the clinical significance and role of circRNAs in gliomas, which is the most common and aggressive primary malignant tumor in the CNS. METHODS: A bioinformatics analysis was performed to profile and screen the dyregulated circRNAs during early neural development. Quantitative real-time PCR was used to detect the expression of circ-MAPK4 and target miRNAs. Glioma cells were transfected with circ-MAPK4 siRNAs, then cell proliferation, apoptosis, transwell assays, as well as tumorigenesis and TUNEL assays, were performed to examine effect of circ-MAPK4 in vitro and vivo. Biotinylated-circ-MAPK4 probe based pull-down assay was conducted to confirm the relationship between circ-MAPK4 and miR-125-3p. RESULTS: In this study, we identified a circRNA, circ-MAPK4 (has_circ_0047688), which was downregulated during early neural differentiation. In gliomas, circ-MAPK4 acted as an oncogene, was inversely upregulated and linked to clinical pathological stage of gliomas (P < 0.05). Next, we verified that circ-MAPK4 promoted the survival and inhibited the apoptosis of glioma cells in vitro and in vivo. Furthermore, we proved that circ-MAPK4 was involved in regulating p38/MAPK pathway, which affected glioma proliferation and apoptosis. Finally, miR-125a-3p, a miRNA exhibited tumor-suppressive function through impairing p38/MAPK pathway, which was increased by inhibiting circ-MAPK4 and could be pulled down by circ-MAPK4. Inhibition of miR-125a-3p could partly rescue the increased phosphorylation levels of p38/MAPK and the elevated amount of apoptosis inducing by knockdown of circ-MAPK4. CONCLUSIONS: Our findings suggest that circ-MAPK4 is a critical player in glioma cell survival and apoptosis via p38/MAPK signaling pathway through modulation of miR-125a-3p, which can serve as a new therapeutic target for treatment of gliomas.

4.
Life Sci ; 245: 117349, 2020 Jan 22.
Artigo em Inglês | MEDLINE | ID: mdl-31981632

RESUMO

AIMS: To explore whether the combination of atorvastatins and resveratrol is superior to each individual drug alone regarding re-endothelialization after drug-eluting stents (DESs) implantation. MATERIALS AND METHODS: Ninety-four rabbits were randomized into control, atorvastatin, resveratrol, and combined medication groups. Abdominal aorta injury was induced via ballooning, followed by DES implantation. Neointimal formation and re-endothelialization after stent implantation were assessed via optical coherence tomography and scanning electron microscopy. The effects of resveratrol and atorvastatin on bone marrow-derived mesenchymal derived stem cells (BMSCs) were assessed. KEY FINDINGS: Compared with the findings in the resveratrol and atorvastatin groups, the neointimal area and mean neointimal thickness were greater in the combined medication group, which also exhibited improved re-endothelialization. Compared with the effects of monotherapy, combined treatment further protected BMSCs against rapamycin-induced apoptosis and improved cell migration. Combined medication significantly upregulated Akt, p-Akt, eNOS, p-eNOS, and CXCR4 expression in BMSCs compared with the effects of monotherapy, and these effects were abolished by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002. SIGNIFICANCE: The combination of atorvastatin and resveratrol has the potential of accelerating re-endothelialization after stent implantation, reducing the risk of thrombosis and improving the safety of DESs.

5.
Per Med ; 17(1): 15-22, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31797717

RESUMO

Aim: This study investigated the association between voriconazole-induced liver injury and gene polymorphisms of CYP2C19 and UGT1A4. Materials & methods: Thirty-eight adult patients who received voriconazole therapy were included in the study. Genotype of CYP2C19 was detected using gene chip hybrid analysis. The UGT1A4 142T>G was genotyped using PCR-RFLP analysis. Results: Ten patients (26.3%) had voriconazole-induced liver injury and were considered as the case group There was no significant difference between the two groups in genotype and allele frequencies of CYP2C19*2 and UGT1A4 142T>G (p > 0.05), however, the GA frequency of CYP2C19 *3 in the drug-induced liver injury case group was higher than that in the control group (p < 0.05). Compared with patients carrying *1/*1 or *1/*2, there was no significant difference in voriconazole trough concentration of the patients with *1/*3 (p > 0.05). Conclusion: There was no significant correlation between voriconazole-induced liver injury and gene polymorphisms of CYP2C19 and UGT1A4.

6.
Nucleic Acids Res ; 48(D1): D307-D313, 2020 Jan 08.
Artigo em Inglês | MEDLINE | ID: mdl-31598693

RESUMO

RNA binding proteins (RBPs) are a large protein family that plays important roles at almost all levels of gene regulation through interacting with RNAs, and contributes to numerous biological processes. However, the complete list of eukaryotic RBPs including human is still unavailable. Here, we systematically identified RBPs in 162 eukaryotic species based on both computational analysis of RNA binding domains (RBDs) and large-scale RNA binding proteomic data, and established a comprehensive eukaryotic RBP database, EuRBPDB (http://EuRBPDB.syshospital.org). We identified a total of 311 571 RBPs with RBDs (corresponding to 6368 ortholog groups) and 3,651 non-canonical RBPs without known RBDs. EuRBPDB provides detailed annotations for each RBP, including basic information and functional annotation. Moreover, we systematically investigated RBPs in the context of cancer biology based on published literatures, PPI-network and large-scale omics data. To facilitate the exploration of the clinical relevance of RBPs, we additionally designed a cancer web interface to systematically and interactively display the biological features of RBPs in various types of cancers. EuRBPDB has a user-friendly web interface with browse and search functions, as well as data downloading function. We expect that EuRBPDB will be a widely-used resource and platform for both the communities of RNA biology and cancer biology.

7.
Eur J Pharmacol ; 868: 172885, 2020 Feb 05.
Artigo em Inglês | MEDLINE | ID: mdl-31870832

RESUMO

The aberrant accumulation of iron causes vascular endothelium damage, which is thought to be associated with excess reactive oxygen species (ROS) generation. Quercetin (Que), as a flavonoid, has a certain ability to scavenge free radicals. Therefore, we aimed to explore the protective mechanism of Que on iron overload induced HUVECs injury focused on ROS/ADMA/DDAHⅡ/eNOS/NO pathway. In this study, HUVECs was treated with 50 µM iron dextran and 20 µM Que for 48 h. We found that Que attenuated the damages induced by iron, as evidenced by decreased ROS generation, increased DDAHⅡexpression and activity, reduced ADMA level, increased NO content and p-eNOS/eNOS ratio, and eventually caused a decrease in apoptosis. After addition of pAD/DDAHⅡ-shRNA, the effects of Que mentioned above were reversed. Meanwhile, iron overload induced mitochondrial oxidative stress, reduced mitochondrial membrane potential and increased mitochondrial permeability transition pores (mPTP) opening, which were also partially alleviated by Que. In addition, L-arginine (L-Arg), a ADMA competition substrate, ciclosporin A (CsA), a mPTP blocking agent, and edaravone (Eda), a free radical scavenger, were used as positive control reagents. The effects of Que were similar to that of L-Arg, CsA and Eda treatment. These results illustrated that Que could attenuate iron overload induced HUVECs mitochondrial dysfunction via ROS/ADMA/DDAHⅡ/eNOS/NO pathway.

8.
J Clin Pharm Ther ; 2019 Dec 04.
Artigo em Inglês | MEDLINE | ID: mdl-31800132

RESUMO

WHAT IS KNOWN AND OBJECTIVE: In the mid-1960s, clinical pharmacy developed in the USA, and as the demand for pharmaceutical services continued to grow, their impact began to be taken seriously. However, the participation of clinical pharmacists as members of the multidisciplinary team in the orthopaedic department is still in its infancy, although its role in orthopaedics has not been defined. The object of this study was to identify and discuss the impact of pharmaceutical care in the orthopaedic department. METHODS: A literature search was conducted on MEDLINE, PubMed, Web of Science, the Cochrane Library and CNKI (China National Knowledge Infrastructure) for papers published between 1998 and 2019, using the keywords pharmacy, pharmacist, and medication or drug combined with orthopaedic. Other available resources were also used to identify relevant articles. RESULTS AND DISCUSSION: Based on the available evidence in 74 articles, it was found that clinical pharmacists play an important role in all aspects of rational use of medications, medication review and reconciliation, monitoring adverse drug events, risk assessment, and medication education and counselling. In addition, clinical pharmacy services were developed to minimize medication errors, adverse drug events and medical costs, but clinical pharmacy is still in its early stages in orthopaedics. WHAT IS NEW AND CONCLUSION: A multidisciplinary approach should be adopted in the orthopaedic department, as pharmacist interventions can be vital for promoting the safety, effectiveness and cost-effectiveness of pharmacotherapy. Although pharmacists' contributions to orthopaedics are not yet fully recognized, pharmaceutical services can undoubtedly contribute to both clinical and societal outcomes.

9.
J Cancer ; 10(27): 6837-6847, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31839818

RESUMO

Regulator of chromosome condensation 2 (RCC2), also known as TD-60, is an RCC1 family member and plays an essential role in mitosis. However, the roles of RCC2 in breast cancer are still unclear. In this study, RCC2 was found to exert oncogenic activities in breast cancer. Samples of breast cancer tissue revealed an increased level of RCC2 and a high level of RCC2 was associated with poor overall survival rate of breast cancer patients. Overexpression of RCC2 significantly enhanced cell proliferation and migration abilities of breast cancer cells in vitro and in vivo. Mechanistically, RCC2 induced epithelial-mesenchymal transition (EMT) through the activation of Wnt signaling pathway. Collectively, our study indicates that RCC2 contributes to breast cancer progression and functions as an important regulator of EMT through the activation of Wnt signaling.

10.
Ying Yong Sheng Tai Xue Bao ; 30(11): 3671-3680, 2019 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-31833679

RESUMO

To explore the nutrient source and supply-demand relationship of the female cone deve-lopment and new shoot growth of Pinus koraiensis, reproductive mother branches were experimentally girdled, defoliated, and under the combination of both treatments. The effects of different treatments on the female cones development, branch growth and the content of carbohydrate (NSC), nitrogen (N) and phosphorus (P) in different tissues and organs were measured. The results showed that girdling significantly affected female cone development, new shoot growth, and the contents of NSC, N and P in different tissues and organs, while defoliation treatment had limited effect. The NSC content in the mother branch xylem and phloem after girdling were significantly lower than that of the control (CK, ungirdling+0% defoliation), and decreased significantly with the increases of the degree of defoliation. The NSC content in mother branch xylem and phloem of girdling+100% defoliation was 59.0% and 64.8% lower than that of CK, respectively. The deficiency of NSC resulted in the death of mother branches and new shoots and the abortion of female cone. Under girdling treatment, the contents of N and P in xylem and phloem of mother branches of 0%, 50% and 100% defoliation treatment were significantly higher than that of CK. The contents of N and P in xylem of mother branches were 17.3%, 18.2% and 24.3% and 17.9%, 7.1% and 3.6% higher than those of CK, respectively. The contents of N and P in phloem of mother branches was 39.3%, 35.2% and 48.9% and 31.0%, 28.2% and 14.8% higher than those of CK, respectively. The female cone development and new shoot growth of P. koraiensis consumed a large amount of NSC, N and P. The carbohydrates and mineral nutrients manufactured or stored in the mother branches could not meet the needs of female cone development and new shoot growth, and thus they need to be imported from other tissues.


Assuntos
Pinus , Feminino , Nitrogênio , Nutrientes , Folhas de Planta , Árvores , Xilema
11.
Artigo em Inglês | MEDLINE | ID: mdl-31876352

RESUMO

OBJECTIVES: To improve the prognostic value of the age, creatinine, and ejection fraction (ACEF) score following percutaneous coronary intervention (PCI) by integrating the residual SYNTAX score (rSS). BACKGROUND: ACEF score was proposed for predicting the operative mortality risk in elective cardiac operations and has been validated in numerous studies. However, it does not incorporate coronary lesion-based variables for risk assessment of patients who undergo PCI. METHODS: Overall, 10,072 patients who underwent PCI at our hospital in 2013 were enrolled. The endpoint was 2-year cardiac death after PCI, defined as death that was not attributed to a non-cardiac cause. ACEF-rSS was constructed with incremental weights attributed to the ACEF score and rSS according to their estimated coefficients. RESULTS: 2-year cardiac death occurred in 63 patients (0.63%). In multivariable analyses, the ACEF score and rSS > 8 were independently associated with the risk of cardiac death. ACEF-rSS was computed as age (years)/ejection fraction (%) + 1 (if creatinine ≥2.0 mg/dl) + 1 (if rSS >8). The discrimination of ACEF-rSS was significantly better than that of the ACEF score based on receiver operating characteristic (ROC) curve analysis and integrated discrimination improvement (IDI) (C-statistics = 0.835 vs. 0.776 for ACEF-rSS and ACEF score, respectively, p = .029; IDI = 0.014, p < .001). Compared with all other SYNTAX-derived risk scores, ACEF-rSS had significantly better discrimination ability based on ROC curve analysis, net reclassification improvement, and IDI. CONCLUSIONS: Combining the ACEF score with rSS to produce the ACEF-rSS enhanced the predictive ability for long-term cardiac mortality.

12.
Oxid Med Cell Longev ; 2019: 5820415, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31885804

RESUMO

Doxorubicin (Dox) with cardiotoxicity and endotheliotoxicity limits its clinical application for cancer. The toxicitic mechanism involves excess ROS generation. 14-3-3s have the protective effects on various injured tissues and cells. Tetramethylpyrazine (TMP) is an alkaloid extracted from the rhizome of Ligusticum wallichii and has multiple bioactivities. We hypothesize that TMP has the protective effects on vascular endothelium by upregulating 14-3-3γ. To test the hypothesis, Dox-induced endotheliotoxicity was used to establish vascular endothelium injury models in mice and human umbilical vein endothelial cells. The effects of TMP were assessed by determining thoracic aortic strips' endothelium-dependent dilation (EDD), as well as LDH, CK, caspase-3, SOD, CAT, GSH-Px activities and MDA level in serum, apoptotic rate, and histopathological changes of vascular tissue (in vivo). Also, cell viability, LDH and caspase-3 activities, ROS generation, levels of NAD+/NADH and GSH/GSSG, MMP, mPTP opening, and apoptotic rate were evaluated (in vitro). The expression of 14-3-3γ and Bcl-2, as well as phosphorylation of Bad (S112), were determined by Western blot. Our results showed that Dox-induced injury to vascular endothelium was decreased by TMP via upregulating 14-3-3γ expression in total protein and Bcl-2 expression in mitochondria, activating Bad (S112) phosphorylation, maintaining EDD, reducing LDH, CK, and caspase-3 activities, thereby causing a reduction in apoptotic rate, and histopathological changes of vascular endothelium (in vivo). Furthermore, TMP increased cell viability and MMP levels, maintained NAD+/NADH, GSH/GSSG balance, decreased LDH and caspase-3 activities, ROS generation, mPTP opening, and apoptotic rate (in vitro). However, the protective effects to vascular endothelium of TMP were significantly canceled by pAD/14-3-3γ-shRNA, an adenovirus that caused knockdown 14-3-3γ expression, or ABT-737, a specific Bcl-2 inhibitor. In conclusion, this study is the first to demonstrate that TMP protects the vascular endothelium against Dox-induced injury via upregulating 14-3-3γ expression, promoting translocation of Bcl-2 to the mitochondria, closing mPTP, maintaining MMP, inhibiting RIRR mechanism, suppressing oxidative stress, improving mitochondrial function, and alleviating Dox-induced endotheliotoxicity.

13.
Oxid Med Cell Longev ; 2019: 2340392, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31781327

RESUMO

It has been recognized that iron overload may harm the body's health. Vascular endothelial cells (VECs) are one of the main targets of iron overload injury, and the mechanism involved was thought to be related to the excessive generation of reactive oxygen species (ROS). However, the subcellular and temporal characteristics of ROS generation, potential downstream mechanisms, and target organelles in VECs injured by iron overload have not been expounded yet. In this study, we elucidated the abovementioned issues through both in vivo and in vitro experiments. Mice were fed pellet diets that were supplemented with iron for 4 consecutive months. Results showed that the thoracic aortic strips' endothelium-dependent dilation was significantly impaired and associated with inflammatory changes, noticeable under brown TUNEL-positive staining in microscopy analysis. In addition, the serum content of asymmetric dimethylarginine (ADMA) increased, whereas nitric oxide (NO) levels decreased. Furthermore, the dimethylarginine dimethylaminohydrolase II (DDAHII) expression and activity, as well as the phosphorylation of endothelial nitric oxide synthase (eNOS) in aortic tissue, were inhibited. Human umbilical vein endothelial cells were treated with 50 µM iron dextran for 48 hours, after which the cell viability, NO content, DDAHII expression and activity, and phosphorylation of eNOS decreased and lactate dehydrogenase and caspase-3 activity, ADMA content, and apoptotic cells significantly increased. After the addition of L-arginine (L-Arg) or pAD/DDAHII, the abovementioned changes were reversed. By dynamically detecting the changes of ROS generation in the cytoplasm and mitochondria and interfering with different aspects of signaling pathways, we have confirmed for the first time that excessive ROS originates from the cytoplasm and activates the ROS-induced ROS release (RIRR) mechanism, leading to mitochondrial dysfunction. Together, our data suggested that excessive free iron ions produced excess ROS in the cytoplasm. Thus, excess ROS create one vicious circle by activating the ADMA/eNOS/DDAHII/NO pathway and another vicious circle by activation of the RIRR mechanism, which, when combined, induce a ROS burst, resulting in mitochondrial dysfunction and damaged VECs.

14.
Cell Biosci ; 9: 89, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31700606

RESUMO

Background: Schizophrenia is a common psychiatric disease with high hereditary. The identification of schizophrenia risk genes (SRG) has shed light on its pathophysiological mechanisms. Mouse genetic models have been widely used to study the function of SRG in the brain with a cell type specific fashion. However, whether the cellular expression pattern of SRG is conserved between human and mouse brain is not thoroughly studied. Results: We analyzed the single-cell transcription of 180 SRG from human and mouse primary visual cortex (V1). We compared the percentage of glutamatergic, GABAergic and non-neuronal cells that express each SRG between mouse and human V1 cortex. Thirty percent (54/180) of SRG had significantly different expression rate in glutamatergic neurons between mouse and human V1 cortex. By contrast, only 5.6% (10/180) of SRG showed significantly different expression in GABAergic neurons, which is similar with the ratio of SRG (15/180) with species difference in total cell populations. Strikingly, the percentage of non-neuronal cells expressing all SRG are indistinguishable between human and mouse V1 cortex. We further analyzed the biological significance of differentially expressed SRG by gene ontology. The species-different SRG in glutamatergic neurons are highly expressed in dendrite and axon. They are enriched in the biological process of response to stimulus. However, the differentially expressed SRG in GABAergic neurons are enriched in the regulation of organelle organization. Conclusion: GABAergic neurons are more conserved in the expression of SRG than glutamatergic neurons while the non-neuronal cells show the species conservation for the expression of all SRG. It should be cautious to use mouse models to study those SRG which show different cellular expression pattern between human and mouse cortex.

15.
BMC Infect Dis ; 19(1): 871, 2019 Oct 22.
Artigo em Inglês | MEDLINE | ID: mdl-31640591

RESUMO

BACKGROUND: On 7th June, 2018, a primary school in Beijing, China notified Shunyi CDC of an outbreak of acute respiratory disease characterized by fever and cough among students and resulting in nine hospitalization cases during the preceding 2 weeks. We started an investigation to identify the etiologic agent, find additional cases, develop and implement control measures. METHODS: We defined probable cases as students, teachers and other staffs in the school developed fever (T ≥ 37.5 °C) with cough or sore throat; or a diagnosis of pneumonia during May 1-June 31, 2018. Confirmed cases were probable cases with Mycoplasma pneumoniae detected in oropharyngeal (OP) swabs by quantitative real-time polymerase chain reaction (qPCR). We searched case by reviewing school absenteeism records and interviewing students, teachers and staff in this school. Oropharyngeal swabs were collected from symptomatic students. Two qPCR) assay, a duplex qPCR assay, and sequencing were performed to determine the pathogen, genotype and macrolide resistance at the gene level, respectively. RESULTS: From May 1st to June 31st, 2018, we identified 55 cases (36 probable and 19 confirmed), of whom 25 (45%) were hospitalized for complications. All cases were students, none of the teachers and other staffs in the school were with similar symptoms. The attack rate (AR) was 3.9% (55/1398) for all students. The cases were mainly male (58%), with an age range of 7-8 years (median: 7 years). 72% (18/25) of inpatients had radiograph findings consistent with pneumonia, and some cases were hospitalized for up to 4 weeks. Pathogen detection results indicated that Mycoplasma pneumonia (M. pneumoniae) P1 type 1 was the causative agent in this outbreak, and the strain harbored one point mutation of A to G at position 2063. CONCLUSIONS: The infections by macrolide-resistant M. pneumoniae are not always mild and pneumonia was common and M. pneumoniae could causes serious complications which require long-term hospitalization. In the future infectious disease prevention and control practice, M. pneumoniae should be paid more attention. It is necessary to establish and improve the pathogen and drug resistance surveillance system in order to prevent and control such mutated strains of M. pneumoniae from causing future outbreaks or epidemics in China.


Assuntos
Antibacterianos/uso terapêutico , Farmacorresistência Bacteriana/genética , Macrolídeos/uso terapêutico , Mycoplasma pneumoniae/efeitos dos fármacos , Pneumonia por Mycoplasma/tratamento farmacológico , Pneumonia por Mycoplasma/epidemiologia , Pequim/epidemiologia , Criança , Tosse/epidemiologia , Surtos de Doenças , Farmacorresistência Bacteriana/efeitos dos fármacos , Feminino , Febre/epidemiologia , Febre/microbiologia , Genótipo , Humanos , Masculino , Mycoplasma pneumoniae/genética , Mycoplasma pneumoniae/patogenicidade , Faringite/epidemiologia , Pneumonia por Mycoplasma/complicações , Mutação Puntual , Reação em Cadeia da Polimerase em Tempo Real , Instituições Acadêmicas , Estudantes
16.
Ecol Evol ; 9(19): 11406-11419, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31641482

RESUMO

Climatic oscillations during the last glacial maximum (LGM) significantly affected the distribution patterns and genetic structure of extant plants. Northeast China (NEC) is a major biodiversity center in East Asia, and the influence of historical climate change on NEC populations is critical for understanding species responses to future climate change. However, only a few phylogeographic studies of cool temperate deciduous tree species have been conducted in the area, and results are inconsistent for species with different niches or distribution areas. We employed multiple chloroplast and nuclear markers to investigate the genetic structure of two ecologically contrasting species, Betula platyphylla and B. ermanii, in NEC. Rare haplotypes were identified in the chloroplast genome of these species, and both exhibited high levels of nucleotide diversity based on a fragment of the nuclear gene G3PDH and microsatellites. Moreover, significant phylogeographic structure was detected for B. platyphylla, suggesting that these populations had recolonized from independent glacial refuges, whereas no genetic structure was found for B. ermanii. OPEN RESEARCH BADGES: The nSSR datasets used in the current study and the table of pairwise FST (below diagonal) and its standardized F'ST (above diagonal) among 25 populations based on seven SSRs are available from the Dryad (DOI: https://doi.org/10.5061/dryad.230d176). Sequences generated from this study were deposited in GenBank under Accession nos. KY199568-KY200162 and MK819541-MK819970.

17.
J Cell Biochem ; 120(12): 19338-19344, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31535398

RESUMO

OBJECTIVE: To explore the role and molecular mechanism of regulatory T (Treg) cells in type 1 diabetes (T1D). METHODS: Patients with T1D and the healthy volunteers were selected and a number of CD3+ , CD4+ , CD25+ , and CD127- T cells were determined. The rats were divided into the control, T1D model, and Treg infusion (T1D rats were infused with Treg) group. The number of CD4+ , CD8- , and CD25+ T cells in the three groups were determined by flow cytometry. Weight, blood glucose, serum insulin, peptide C, glucagon, and glucagon like peptide 1 in the three groups were also determined. The messenger RNA (mRNA) levels and contents of interleukin (IL)-10, IL-4, transforming growth factor (TGF)-ß, IL-2, IL-17, and IFN-γ in patients with T1D, healthy volunteers, streptozotocin (STZ)-induced T1D rat model, the control rat, and Treg infusion rats were determined by reverse transcription polymerase chain reaction and the enzyme-linked immunosorbent assay, respectively. RESULTS: Treg content in patients with T1D was significantly decreased compared with the control volunteers. Treg content in rats was markedly decreased after injection with STZ to induce T1D rat model, while Treg infusion weakened the decrease. The change scope of weight and blood glucose in the model and Treg group was bigger than the control group, and the change in the infusion group was lighter than the model group. T1D decreased the expressions of IL-10, IL-4, TGF-ß, and IL-2, while Treg infusion weakened the decrease. The expressions of IL-17 and IFN-γ in the T1D group was increased, while Treg infusion weakened the increase. CONCLUSION: Autologous Treg infusion can strengthen the immunologic and islet function to treat T1D which may be via regulating the expression of inflammatory factors.

18.
Appl Opt ; 58(18): 5107-5114, 2019 Jun 20.
Artigo em Inglês | MEDLINE | ID: mdl-31503832

RESUMO

The operational reliability directly affects the practical application of optical current transformers (OCTs) in smart substations. As the key component of the OCT, the reliability of the optical current sensor (OCS) largely determines the reliability level of the OCT. This paper proposes a reliability assessment method of the OCS based on accelerated aging tests. The failure modes and failure mechanisms of the OCS are analyzed, and the concept of OCS insertion loss variation is proposed. An allowable range of insertion loss variation is selected as the failure criterion of the OCS. From the viewpoint of the OCS measurement error generated by the quantization error of the analog-to-digital converter, the allowable range of insertion loss variation is obtained. By selecting a high temperature as the accelerated thermal stress, we design the accelerated aging test scheme of the OCS and analyze the sample test data to obtain the activation energy of the OCS insertion loss failure. Based on this activation energy, the median time to failure and instantaneous failure rate curve of the OCS at normal temperature are obtained. The results indicate that the designed OCS has an expected service life of 50 years and a low instantaneous failure rate at normal temperature. This paper provides basic critical reliability analysis data for the system reliability assessment of OCTs.

19.
Sci Rep ; 9(1): 12661, 2019 Sep 02.
Artigo em Inglês | MEDLINE | ID: mdl-31477771

RESUMO

Cassava (Manihot esculenta) is a major staple food, animal feed and energy crop in the tropics and subtropics. It is one of the most drought-tolerant crops, however, the mechanisms of cassava drought tolerance remain unclear. Abscisic acid (ABA)-responsive element (ABRE)-binding factors (ABFs) are transcription factors that regulate expression of target genes involved in plant tolerance to drought, high salinity, and osmotic stress by binding ABRE cis-elements in the promoter regions of these genes. However, there is little information about ABF genes in cassava. A comprehensive analysis of Manihot esculenta ABFs (MeABFs) described the phylogeny, genome location, cis-acting elements, expression profiles, and regulatory relationship between these factors and Manihot esculenta betaine aldehyde dehydrogenase genes (MeBADHs). Here we conducted genome-wide searches and subsequent molecular cloning to identify seven MeABFs that are distributed unevenly across six chromosomes in cassava. These MeABFs can be clustered into three groups according to their phylogenetic relationships to their Arabidopsis (Arabidopsis thaliana) counterparts. Analysis of the 5'-upstream region of MeABFs revealed putative cis-acting elements related to hormone signaling, stress, light, and circadian clock. MeABF expression profiles displayed clear differences among leaf, stem, root, and tuberous root tissues under non-stress and drought, osmotic, or salt stress conditions. Drought stress in cassava leaves and roots, osmotic stress in tuberous roots, and salt stress in stems induced expression of the highest number of MeABFs showing significantly elevated expression. The glycine betaine (GB) content of cassava leaves also was elevated after drought, osmotic, or salt stress treatments. BADH1 is involved in GB synthesis. We show that MeBADH1 promoter sequences contained ABREs and that MeBADH1 expression correlated with MeABF expression profiles in cassava leaves after the three stress treatments. Taken together, these results suggest that in response to various dehydration stresses, MeABFs in cassava may activate transcriptional expression of MeBADH1 by binding the MeBADH1 promoter that in turn promotes GB biosynthesis and accumulation via an increase in MeBADH1 gene expression levels and MeBADH1 enzymatic activity. These responses protect cells against dehydration stresses by preserving an osmotic balance that enhances cassava tolerance to dehydration stresses.

20.
EuroIntervention ; 2019 Aug 13.
Artigo em Inglês | MEDLINE | ID: mdl-31403461

RESUMO

AIMS: To use optical coherence tomography (OCT) to predict newly implanted stent expansion for treatment of in-stent restenosis (ISR). METHODS AND RESULTS: With OCT-guidance, 143 ISR lesions were treated with a new stent. Stent underexpansion was defined as minimum stent area (MSA) <4.5mm 2 and MSA/average of reference lumen area <70%. New stent underexpansion was found in 33 lesions (23%), had a smaller old stent MSA (4.13 [3.32-4.62] versus 5.18 [4.01-6.38] mm 2 , p=0.001), and had a higher prevalence of multiple old stent layers (51.5% versus 10.9%, p<0.001) and neointimal or peri-stent calcium (69.7% versus 37.3%, p=0.001) compared to those without new stent underexpansion. Old stent underexpansion, multiple layers of old stent, maximum calcium angle >180°, and maximum calcium thickness >0.5mm were independently associated with new stent underexpansion. Patients with new stent underexpansion had a higher prevalence of major adverse cardiac events (35.5% vs 14.3%, p=0.009) mainly driven by a higher rate of myocardial infarction and target vessel revascularization at 2 years. CONCLUSIONS: When re-stenting an ISR lesion, old stent underexpansion, the amount of neointimal or peri-stent calcium, and multiple old stent strut layers are important determinants of new stent underexpansion that is then associated with adverse long-term outcomes.

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