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1.
Nurse Educ Today ; : 104655, 2020 Nov 28.
Artigo em Inglês | MEDLINE | ID: mdl-33303246

RESUMO

OBJECTIVES: We aimed to (1) evaluate the effectiveness of virtual reality (VR) training in improving knowledge among nursing students and (2) identify the essential features of training. DESIGN: This systematic review was conducted according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines. DATA SOURCES: Randomised controlled trials (RCTs) were obtained from PubMed, EMBASE, Cochrane Library, PsycINFO, Cumulative Index to Nursing and Allied Health Literature, ProQuest and Scopus databases from inception up until 15 October 2019. REVIEW METHODS: Meta-analysis and random-effects meta-regression was performed using the Comprehensive Meta-analysis 3.0 software. The overall effect was measured using Hedges' g and determined using Z-statistics at the significance level of p < 0.05. Heterogeneity was assessed using χ2 and I2 statistics. The risk of bias tool and the Grading of the Recommendation, Assessment, Development and Evaluation (GRADE) system were employed to assess individual and overall quality of evidence, respectively. RESULTS: Among the 1993 records identified, 14 trials were included. Meta-analysis demonstrated a significant improvement in knowledge, with a small-to-medium effect (g = 0.47) in the VR group compared to the control group (Z = 2.66, p = 0.01). Subgroup analyses highlighted that VR training was more efficacious in delivering procedural knowledge to undergraduate nursing students when conducted in multiple, self-guided, short sessions within 30 min and by using low-moderate level of immersion. Meta-regression did not detect significant covariates that influenced knowledge scores. CONCLUSIONS: Virtual reality may be a viable teaching strategy to improve knowledge acquisition, but it is presently suitable for supplementing conventional teaching methods. Nonetheless, VR could complement current pedagogy to address challenges associated with decreased clinical placement opportunities. Larger, well-designed RCTs are required to strengthen the evidence about the effectiveness of VR training.

2.
Plant Signal Behav ; 15(12): 1836883, 2020 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-33100175

RESUMO

The circadian clock is a universal timing system that involved in plant physical responses to abiotic stresses. Moreover, OSCA1 is an osmosensor responsible for [Ca2+]i increases induced by osmotic stress in plants. However, there is little information on osmosensor involved osmotic stress-triggered circadian clock responses. Using an aequorin-based Ca2+ imaging assay, we found the gradient (0 mM, 200 mM, 500 mM) osmotic stress (induced by sorbitol) both altered the primary circadian parameter of WT and osca1 mutant. This means the plant switch to a fast day/night model to avoid energy consumption. In contrast, the period of WT and osca1 mutant became short since the sorbitol concentration increased from 0 mM to 500 mM. As the sorbitol concentration increased, the phase of the WT becomes more extensive compared with osca1 mutant, which means WT is more capable of coping with the environmental change. Moreover, the amplitude of WT also becomes broader than osca1 mutant, especially in high (500 mM) sorbitol concentration, indicate the WT shows more responses in high osmotic stress. In a word, the WT has much more flexibility to cope with the osmotic stress than osca1 mutant. It implies the OSCA1 might be involved in the circadian gated plant adaptation to the environmental osmotic stress, which opens an avenue to study Ca2+ processes with other circadian signaling pathways.

3.
Medicine (Baltimore) ; 99(44): e22861, 2020 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-33126329

RESUMO

The lack of effective markers leads to missed optimal treatment times, resulting in poorer prognosis in most cancers. Drosophila mothers against decapentaplegic protein (SMAD) family members are important cytokines in the transforming growth factor-beta family. They jointly regulate the processes of cell growth, differentiation, and apoptosis. However, the expression of SMAD family genes in pan-cancers and their impact on prognosis have not been elucidated. Perl software and R software were used to perform expression analysis and survival curve analysis on the data collected by TCGA, GTEx, and GEO, and the potential regulatory pathways were determined through gene ontology enrichment and kyoto encyclopedia of genes and genomes enrichment analysis. It was found that SMAD7 and SMAD9 expression decreased in lung adenocarcinoma (LUAD), and their expression was positively correlated with survival time. Additionally, SMAD7 could be used as an independent prognostic factor for LUAD. In general, SMAD7 and SMAD9 can be used as prognostic markers of LUAD. Further, SMAD7 is expected to become a therapeutic target for LUAD.


Assuntos
Adenocarcinoma de Pulmão/genética , Prognóstico , Proteína Smad7/análise , Biomarcadores Tumorais/análise , Biomarcadores Tumorais/sangue , Expressão Gênica/genética , Humanos , Proteína Smad7/sangue
4.
Artigo em Inglês | MEDLINE | ID: mdl-33082815

RESUMO

Background: Colla Cornus Cervi (CCC) has been used as a traditional Chinese medicine in the treatment of osteoporosis and osteonecrosis of the femoral head. However, the bioavailability of CCC is seriously limited owing to its large molecular weight and complex ingredients. In the present study, antler polypeptide was separated from CCC, and the effects of antler polypeptide on rat bone marrow mesenchymal stem cells (BMSCs) were investigated. Methods: Antler polypeptide was separated from Colla Cornus Cervi by ultrafiltration into different samples according to the molecular weight. The total peptide content of these samples was determined by the biuret method. The content of antler polypeptide in different samples was quantified by high-performance liquid chromatography (HPLC). The effects of antler polypeptide at different concentrations on the proliferation, cell cycle, alkaline phosphatase activity, and BMP7 expression of BMSCs were investigated. Results: Antler polypeptide was separated by ultrafiltration into different samples: A (molecular weight <800 Da), B (molecular weight 800-1500 Da), and C (molecular weight >1500 Da). The total peptide contents of A, B, and C were 0.602 mg/mL, 8.976 mg/mL, and 38.88 mg/mL. Antler polypeptide B eluted at 14.279∼15.351 min showed that the content of antler polypeptide was significantly higher than that of A and C with a peak area of 933.80927. The BMSCs proliferation rate (84.66%) of polypeptide B was the highest at the concentration of 1.578 × 10-2 g/mL. Antler polypeptide B significantly promoted the proliferation of BMSCs with a proliferation index of 38.68%, which was significantly higher than that of the other groups. Antler polypeptide B significantly enhanced the activity of alkaline phosphatase in BMSCs compared to that of the blank group (P < 0.001). Antler polypeptide B increased the BMP7 protein expression in BMSCs. Conclusions: Results suggested that antler polypeptide may promote the proliferation and osteogenic differentiation of BMSCs. Our study lays an experimental foundation for the further development and application of antler polypeptide in medicine.

5.
Appl Environ Microbiol ; 86(23)2020 11 10.
Artigo em Inglês | MEDLINE | ID: mdl-32978127

RESUMO

Long-term nitrogen field fertilization often results in significant changes in nitrifying communities that catalyze a key step in the global N cycle. However, whether microcosm studies are able to inform the dynamic changes in communities of ammonia-oxidizing bacteria (AOB) and archaea (AOA) under field conditions remains poorly understood. This study aimed to evaluate the transcriptional activities of nitrifying communities under in situ conditions, and we found that they were largely similar to those of 13C-labeled nitrifying communities in the urea-amended microcosms of soils that had received different N fertilization regimens for 22 years. High-throughput sequencing of 16S rRNA genes and transcripts suggested that Nitrosospira cluster 3-like AOB and Nitrososphaera viennensis-like AOA were significantly stimulated in N-fertilized fresh soils. Real-time quantitative PCR demonstrated that the significant increase of AOA and AOB in fresh soils upon nitrogen fertilization could be preserved in the air-dried soils. DNA-based stable-isotope probing (SIP) further revealed the greatest labeling of Nitrosospira cluster 3-like AOB and Nitrosospira viennensis-like AOA, despite the strong advantage of AOB over AOA in the N-fertilized soils. Nitrobacter-like nitrite-oxidizing bacteria (NOB) played more important roles than Nitrospira-like NOB in urea-amended SIP microcosms, while the situation was the opposite under field conditions. Our results suggest that long-term fertilization selected for physiologically versatile AOB and AOA that could have been adapted to a wide range of substrate ammonium concentrations. It also provides compelling evidence that the dominant communities of transcriptionally active nitrifiers under field conditions were largely similar to those revealed in 13C-labeled microcosms.IMPORTANCE The role of manipulated microcosms in microbial ecology has been much debated, because they cannot entirely represent the in situ situation. We collected soil samples from 20 field plots, including 5 different treatments with and without nitrogen fertilizers for 22 years, in order to assess active nitrifying communities by in situ transcriptomics and microcosm-based stable-isotope probing. The results showed that chronic N enrichment led to competitive advantages of Nitrosospira cluster 3-like AOB over N. viennensis-like AOA in soils under field conditions. Microcosm labeling revealed similar results for active AOA and AOB, although an apparent discrepancy was observed for nitrite-oxidizing bacteria. This study suggests that the soil microbiome represents a relatively stable community resulting from complex evolutionary processes over a large time scale, and microcosms can serve as powerful tools to test the theory of environmental filtering on the key functional microbial guilds.


Assuntos
Archaea/isolamento & purificação , Bactérias/isolamento & purificação , Nitrogênio/metabolismo , Microbiologia do Solo , Archaea/genética , Bactérias/genética , Fertilizantes/análise , Perfilação da Expressão Gênica , Sequenciamento de Nucleotídeos em Larga Escala , RNA Arqueal/análise , RNA Bacteriano/análise , RNA Ribossômico 16S/análise , Reação em Cadeia da Polimerase em Tempo Real , Transcrição Genética
6.
Neural Plast ; 2020: 9260807, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32908492

RESUMO

Waardenburg syndrome (WS), also known as auditory-pigmentary syndrome, is the most common cause of syndromic hearing loss. It is responsible for 2-5% of congenital deafness. WS is classified into four types depending on the clinical phenotypes. Currently, pathogenic mutation of PAX3, MITF, EDNRB, EDN3, SNAI2, or SOX10 can cause corresponding types of WS. Among them, SOX10 mutation is responsible for approximately 15% of type II WS or 50% of type IV WS. We report the case of a proband in a Chinese family who was diagnosed with WS type II. Whole exome sequencing (WES) of the proband detected a novel heterozygous spontaneous mutation: SOX10 c.246delC. According to analysis based on nucleic acid and amino acid sequences, this mutation may produce a truncated protein, with loss of the HMG structure domain. Therefore, this truncated protein may fail to activate the expression of the MITF gene, which regulates melanocytic development and plays a key role in WS. Our finding expands the database of SOX10 mutations associated with WS and provides more information regarding the molecular mechanism of WS.

7.
Ann Thorac Surg ; 2020 Aug 20.
Artigo em Inglês | MEDLINE | ID: mdl-32828749

RESUMO

We report one case of 21-year-old man with a cardiac pheochromocytoma involving the right atrium and extending to the right ventricular inflow tract, which was diagnosed by somatostatin receptor scintigraphy. For preoperative evaluation, we chose multimodalities imaging for accurate describing the anatomic extent and location of the tumor and its surrounding tissues, it showed that no major coronary artery run through the tumor. The tumor was resected with disease-free margins effectively and safely with the use of cardiopulmonary bypass and with cardiac arrest. The patient remain asymptomatic at 3-month follow-up.

8.
Endocrine ; 70(3): 607-615, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32816205

RESUMO

PURPOSE: Apparent mineralocorticoid excess (AME) is an ultrarare autosomal recessive disorder resulting from deficiency of 11ß-hydroxysteroid dehydrogenase type 2 (11ßHSD2) caused by mutations in HSD11B2. The purpose of this study was to identify novel compound heterozygous HSD11B2 mutations in a Chinese pedigree with AME and conduct a systematic review evaluating the AME clinical features associated with HSD11B2 mutations. METHODS: Next-generation sequencing was performed in the proband, and Sanger sequencing was used to identify candidate variants in family members, 100 hypertensives, and 100 healthy controls. A predicted structure of 11ßHSD2 was constructed by in silico modeling. A systematic review was used to identify cases of HSD11B2-related AME. Data for genotyping and clinical characterizations and complications were extracted. RESULTS: Next-generation sequencing showed novel compound heterozygous mutations (c.343_348del and c.1099_1101del) in the proband with early-onset hypertension and hypokalemia. Sanger sequencing verified the monoallelic form of the same mutations in five other relatives but not in 100 hypertensives or 100 healthy subjects. In silico structural modeling showed that compound mutations may simultaneously perturb the substrate and coenzyme binding pocket. A systematic review of 101 AME patients with 54 HSD11B2 mutations revealed early-onset hypertension, hypokalemia and homozygous mutations as common features. The homozygous HSD11B2 mutations correlated with low birth weight (r = 0.285, P = 0.02). CONCLUSIONS: We report novel compound heterozygous HSD11B2 mutations in a Chinese teenager with early-onset hypertension, and enriched genotypic and phenotypic spectrums in AME. Genetic testing helps early diagnosis and treatment for AME patients, which may avoid target organ damage.

9.
Cell Commun Signal ; 18(1): 107, 2020 07 09.
Artigo em Inglês | MEDLINE | ID: mdl-32646440

RESUMO

BACKGROUND: Foxp3+CD4+ regulatory T cells (Treg) constitutes a key event in autoimmune diseases. STAT5b is the critical link between the IL-2/15 and FOXP3, the master regulator of Treg cells. METHODS: The CD3+T cell and Foxp3+CD4+ regulatory T cells were overexpressioned or knockdown MKL-1 and STAT5a and tested for Treg cell development and function. Direct interaction of MKL-1 and STAT5a were analyzed by coimmunoprecipitation assays, Luciferase assay, Immunofluoresence Staining and Yeast two-hybrid screening. The effect of MKL-1 and STAT5a on the Treg genes expression was analyzed by qPCR and western blotting and Flow cytometry. RESULTS: However, the molecular mechanisms mediating STAT5b-dependent Treg genes expression and Treg cell phenotype and function in autoimmune diseases are not well defined. Here, we report that the MKL-1 is a coactivator for the major Treg genes transcription factor STAT5b, which is required for human Treg cell phenotype and function. The N terminus of STAT5b, which contains a basic coiled-coil protein-protein interaction domain, binds the C-terminal activation domain of MKL-1 and enhances MKL-1 mediated transcriptional activation of Treg-specific, CArG containing promoters, including the Treg-specific genes Foxp3. Suppression of endogenous STAT5b expression by specific small interfering RNA attenuates MKL-1 transcriptional activation in cultured human cells. The STAT5b-MKL-1 interaction identifies a role of Treg-specific gene regulation and regulated mouse Treg cell development and function and suggests a possible mechanism for the protective effects of autoimmune disease Idiopathic Thrombocytopenic Purpura (ITP). CONCLUSIONS: Our studies demonstrate for the first time that MKL-1 is a coactivator for STAT5b, the regulator of Treg cell development and function. Video abstract.

10.
Gastroenterol Rep (Oxf) ; 8(3): 252, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32665857

RESUMO

[This corrects the article DOI: 10.1093/gastro/goz038.][This corrects the article DOI: 10.1093/gastro/goz038.].

11.
Huan Jing Ke Xue ; 41(6): 2812-2821, 2020 Jun 08.
Artigo em Chinês | MEDLINE | ID: mdl-32608798

RESUMO

To investigate the potential interference of dead bacteria DNA on the analysis of antibiotic resistance genes (ARGs) and microbial communities in anaerobic digestion sludge, three different types of anaerobic digestion sludge were treated with propidium monoazide (PMA) in this study, and the results of subsequent ARGs and microbial community analysis with the interference of dead cell DNA blocked by PMA was compared to that without PMA treatment. It was found that after PMA treatment, the absolute abundance of the ARGs in the anaerobic digestion sludge from self-anaerobic digestion system of excess sludge and from high solid sludge anaerobic digestion system decreased by 41%-86%, and 74%-98%, respectively. ARGs abundance in the sludge from the anaerobic digestion system with sludge hydrolyzate as a substrate and anaerobic granular sludge as inoculum after 15 days of digestion considerably decreased with PMA treatment. However, its ARGs abundance still declined by up to 34%. PMA treatment influenced the analysis of microbial community of the three types of anaerobic digestion sludge to different degrees, in which the influence was the highest on the community structure analysis of the sludge from high solid anaerobic digestion system. The results of the correlation analysis between the ARGs abundance and the microbial community composition were completely different in the case with PMA treatment and without PMA treatment. This study proved the potential interference of dead cell DNA on the analysis of ARGs and microbial community in anaerobic digestion sludge. PMA pretreatment could achieve a more accurate analysis of the microbial community and ARGs characteristics in anaerobic digestion sludge.


Assuntos
Microbiota/efeitos dos fármacos , Esgotos , Anaerobiose , Antibacterianos/farmacologia , Resistência Microbiana a Medicamentos , Genes Bacterianos/efeitos dos fármacos
12.
Kidney Blood Press Res ; 45(4): 603-611, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32698182

RESUMO

INTRODUCTION: Liddle syndrome (LS), an autosomal dominant and inherited monogenic hypertension syndrome caused by pathogenic mutations in the epithelial sodium channel (ENaC) genes SCNN1A, SCNN1B, and SCNN1G. OBJECTIVE: This study was designed to identify a novel SCNN1B missense mutation in a Chinese family with a history of stroke, and to confirm that the identified mutation is responsible for LS in this family. METHODS: DNA samples were collected from the proband and 11 additional relatives. Next-generation sequencing was performed in the proband to find candidate variants. In order to exclude genetic polymorphism, the candidate variantin SCNN1B was verified in other family members, 100 hypertensives, and 100 healthy controls by Sanger sequencing. RESULTS: Genetic testing revealeda novel and rare heterozygous variant in SCNN1B in the proband. This variant resulted in a substitution of threonine instead of proline at codon 617, altering the PY motif of ß-ENaC. The identified mutation was only verified in 5 relatives. In silico analyses indicated that this variant was highly pathogenic. In this family, phenotypic heterogeneity was present among 6 LS patients. Tailored medicine with amiloride was effective in controlling hypertension and improving the serum potassium concentration in patients with LS. CONCLUSIONS: We identified a novel SCNN1B mutation (c.1849C>A) in a family affected by LS. Patients with LS, especially those with severe hypertension, should be alert for the occurrence of premature stroke. Timely diagnosis using genetic testing and tailored treatment with amiloride can help LS patients to avoid severe complications.

13.
Clin Lab ; 66(6)2020 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-32538045

RESUMO

BACKGROUND: Pertussis, caused by Bordetella pertussis (B. pertussis), is a highly transmissible, acute respiratory disease that occurs in many countries. Diagnosis of pertussis continues to be a challenge using traditional tests due to their turn-around time and sensitivity. Herein, we rapidly and accurately screened a family cluster of pertussis from a child and her mother. METHODS: We used an automated nested multiplex PCR system which included B. pertussis, influenza A virus, and 19 other respiratory pathogens. RESULTS: We detected B. pertussis, influenza A virus H1-2009 (FluA-2009), adenovirus, and respiratory syncytial virus (RSV) in the child, and the mother of the child was positive for B. pertussis and FluA-2009. CONCLUSIONS: Active and timely screening for pertussis of adult family members should be considered. The detection of multiple respiratory pathogens may guide effective antibiotic therapies. This could be a novel test for the prevention of pertussis.

14.
Neural Plast ; 2020: 3569359, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32508908

RESUMO

Jervell and Lange-Nielsen syndrome (JLNS) is a rare but severe autosomal recessive disease characterized by profound congenital deafness and a prolonged QTc interval (greater than 500 milliseconds) in the ECG waveforms. The prevalence of JLNS is about 1/1000000 to 1/200000 around the world. However, exceed 25% of JLNS patients suffered sudden cardiac death with kinds of triggers containing anesthesia. Approximately 90% of JLNS cases are caused by KCNQ1 gene mutations. Here, using next-generation sequencing (NGS), we identified a compound heterozygosity for two mutations c.1741A>T (novel) and c.477+5G>A (known) in KCNQ1 gene as the possible pathogenic cause of JLNS, which suggested a high risk of cardiac events in a deaf child. The hearing of this patient improved significantly with the help of cochlear implantation (CI). But life-threatening arrhythmias occurred with a trigger of anesthesia after the end of the CI surgery. Our findings extend the KCNQ1 gene mutation spectrum and contribute to the management of deaf children diagnosed with JLNS for otolaryngologists (especially cochlear implant teams).

16.
Bioprocess Biosyst Eng ; 43(10): 1869-1883, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32447514

RESUMO

To enhance specific or total sophorolipids (SLs) production by Starmerella bombicola for specific application, mutant library consisting of 106 mutants from 7 batches was constructed via atmospheric and room-temperature plasma (ARTP). When compared to the wild strain, 11, 36 and 12 mutants performed increases over 30% in lactonic, acidic or total SLs production. Genetic stability investigation showed that 8, 7, and 4 mutants could maintain the improved SLs production capacity. Mutants of A6-9 and A2-8 were selected out for enhanced specific SLs and total SLs production in fed-batch cultivation in flask. Without optimization, A6-9 obtained the highest reported lactonic SLs production of 51.95 g/l and A2-8 performed comparable acidic and total SLs production of 68.75 g/l and 100.33 g/l with all the reported stains. The structural composition of the obtained SLs was analyzed by HPLC and LC/MS, and the results confirmed the enhancement of SLs and certain SL components. These mutants would be important in industrial applications because the production and purification costs of SLs could be greatly reduced. Besides, the acquisition of these mutants also provided materials for the investigation of regulation mechanism of SLs biosynthesis for further genetic engineering of S. bombicola. Furthermore, critical micelle concentration (CMC), minimum surface tension (STmin) and hydrophilic-lipophilic balance (HLB) of the SLs obtained from the wild and mutant strains were also examined and compared. These results demonstrated the feasibility of obtaining SLs with different properties from different strains and the high efficiency of mutation breeding of S. bombicola by ARTP.

17.
Gastroenterol Rep (Oxf) ; 8(1): 66-75, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-32257220

RESUMO

Background: Matrix Gla protein (MGP) is a secreted protein contributed to the immunomodulatory functions of mesenchymal stromal cells. Microarray profiling found a significantly higher expression level of the extracellular matrix gene MGP in patients with ulcerative colitis (UC). However, little is known about the role of MGP in UC and its upstream signaling regulation. This study aimed to identify the expression of MGP in UC and its upstream regulator mechanism. Methods: Colonic mucosa biopsies were obtained from patients with UC and healthy controls. DNA microarray profiling was used to explore underlying genes correlating with UC development. Mice were fed with water containing different concentrations of dextran sodium sulfate (DSS) to induce an experimental colitis model. Colonic tissues were collected and evaluated using immunohistochemistry, immunoblot, real-time polymerase chain reaction, and chromatin immunoprecipitation assay. Bioinformatics analysis was performed to identify candidate MGP gene-promoter sequence and transcription-initiation sites. Luciferase-reporter gene assay was conducted to examine the potential transcription factor of MGP gene expression. Results: The expression of MGP was significantly increased in colonic tissues from UC patients and DSS-induced colitis models, and was positively correlated with disease severity. Bioinformatics analysis showed a conserved binding site for Egr-1 in the upstream region of human MGP gene. The significantly higher level of Egr-1 gene expression was found in UC patients than in healthy controls. The activity of luciferase was significantly enhanced in the Egr-1 expression plasmid co-transfected group than in the control group and was further inhibited when co-transfected with the Egr-1 binding-site mutated MGP promoter. Conclusions: Up-regulated expression of MGP was found in UC patients and DSS-induced colitis. The expression of MGP can be regulated by Egr-1.

18.
Neoplasia ; 22(5): 220-230, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32315812

RESUMO

PURPOSE: miR-5100 participates in the proliferation of lung cancer and pancreatic cancer cells, and participates in the differentiation of osteoblasts. However, the regulation of gastric cancer cells in gastric cancer cells remains unclear. EXPERIMENTAL DESIGN: The blood of patients was collected to detect the expression level of miR-5100, and the apoptosis and autophagy levels of cells were detected using western blot, flow cytometry, and confocal. At the same time, in vitro tumor formation experiments in nude mice were used to verify the results of in vitro experiments. RESULTS: The expression of miR-5100 is related to the prognosis of gastric cancer, miR-5100 can enhance the apoptosis level of gastric cancer cells and inhibit the occurrence of autophagy by targeting CAAP1. MKL1 can inhibit the apoptosis of gastric cancer cells and promote the occurrence of autophagy by targeting CAAP1. At the same time, MKL1 can also increase the expression of miR-5100. CONCLUSIONS: Our research reveals the mechanism by which the MKL1/miR-5100/CAAP1 loop regulates apoptosis and autophagy levels in gastric cancer cells, and miR-5100 is expected to become a new potential target for gastric cancer treatment.

19.
Am J Hypertens ; 33(7): 670-675, 2020 07 18.
Artigo em Inglês | MEDLINE | ID: mdl-32161960

RESUMO

BACKGROUND: Liddle syndrome (LS), an autosomal dominant disorder, is a common monogenic hypertension in pediatrics. In this study, we reported a novel SCNN1G variant in a Chinese family with pediatric LS, and conduct a systematic review of epithelial sodium channel (ENaC)-gene-positive LS cases to conclude the clinical genetic features of LS in childhood. METHODS: Next-generation sequencing and in silico analysis were performed in the proband to discover candidate variants. Sanger sequencing was used to identify the predicted likely pathogenic variant. LS patients in this family were treated with amiloride. The Medline database was searched to summarize clinical features of pediatric LS cases whose age at genetic diagnosis was not more than 18 years. RESULTS: Genetic analysis identified a novel SCNN1G missense variant (c.1874C>T, p.Pro625Leu) in the proband with LS in childhood. In silico analysis revealed this heterozygous variant was highly conserved and deleterious. A total of 38 publications described pediatric LS associated with 25 pathogenic variants in SCNN1B and SCNN1G in 54 children. Despite the phenotypic heterogeneity, early-onset hypertension is the most common feature. All LS patients in this family or the reviewed cases showed significantly improvements in hypertension and hypokalemia after treatment with ENaC inhibitors. CONCLUSIONS: This study identified a novel SCNN1G missense variant in a patient with pediatric LS, expanding the genetic spectrum of SCNN1G and demonstrating the PY motif of γ-ENaC as a potential mutant region. Early identification and specific management of LS in children and adolescents are important to prevent the development of hypertensive end-organ disease.

20.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao ; 42(1): 47-54, 2020 Feb 28.
Artigo em Chinês | MEDLINE | ID: mdl-32131939

RESUMO

Objective To investigate the application of Acute Gastrointestinal Injury(AGI) grading in evaluating gastrointestinal failure in patients with acute pancreatitis(AP). Methods In this retrospective observational study,patients presented with moderate severe AP and severe AP in our hospital from October 2013 to October 2016 were consecutively enrolled.Logistic regression analysis and receiver operating characteristic curve were used to explore and evaluate potential predictors of gastrointestinal failure. Results A total of 202 patients were included in this study,with 90 cases(44.6%) identified as gastrointestinal failure.Survival curve showed significantly increased risk of death in patients with gastrointestinal failure(P < 0.05).Logistic regression analysis showed age(OR=1.06,95%CI:1.03-1.09,P<0.001),complaint of stopping flatus and defecation(OR=7.02,95%CI:2.08-23.66,P=0.002),increased counts of white blood cells in peripheral blood(OR=1.09,95%CI:1.02-1.17,P=0.015),decreased level of serum albumin(OR=0.93,95%CI:0.86-1.00,P=0.048),and increased level of serum creatinine at admission(OR=1.02,95%CI:1.01-1.04,P=0.001) were the independent risk factors of gastrointestinal failure.The area under curves of Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) and Beside Index for Severity in Acute Pancreatitis (BISAP) scores in diagnosing gastrointestinal failure were 0.999 and 0.782,respectively. Conclusions Gastrointestinal failure can remarkably increase the risk of death in patients with AP.Both APACHE Ⅱ and BISAP scores at admission are useful in diagnosing gastrointestinal failure in patients with AP.


Assuntos
Gastroenteropatias/diagnóstico , Pancreatite/complicações , APACHE , Doença Aguda , Área Sob a Curva , Diagnóstico Precoce , Gastroenteropatias/complicações , Humanos , Valor Preditivo dos Testes , Prognóstico , Curva ROC , Estudos Retrospectivos , Índice de Gravidade de Doença
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