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1.
Theranostics ; 10(24): 11339-11358, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33042286

RESUMO

Background: TSTA3 gene encodes an enzyme responsible for synthesis of GDP-L-fucose as the only donor in fucosylation. This study was designed to explore clinical value, function and underlying mechanism of TSTA3 in the development of esophageal squamous cell carcinoma (ESCC). Methods: Whole genomic sequencing data from 663 ESCC patients and RNA sequencing data from 155 ESCC patients were used to analyze the copy number variation and mRNA expression of TSTA3 respectively. Immunohistochemistry based or not based on the tissue microarrays was used to detect its protein expression. Transwell assay and in vivo metastasis assay were used to study the effect of TSTA3 on invasion and metastasis of ESCC. Immunofluorescence was used to analyze fucosylation level. N-glycoproteomics and proteomics analysis, Lens Culinaris Agglutinin (LCA) and Ulex Europaeus Agglutinin I (UEA-I) affinity chromatography, immunoprecipitation, glycosyltransferase activity kit and rescue assay were used to explore the mechanism of TSTA3. Results: TSTA3 was frequently amplified and overexpressed in ESCC. TSTA3 amplification and protein overexpression were significantly associated with malignant progression and poor prognosis of ESCC patients. TSTA3 knockdown significantly suppressed ESCC cells invasion and tumor dissemination by decreasing fucosylation level. Conversely, exogenous overexpression of TSTA3 led to increased invasion and tumor metastasis in vitro and in vivo by increasing fucosylation level. Moreover, core fucosylated LAMP2 and terminal fucosylated ERBB2 might be mediators of TSTA3-induced pro-invasion in ESCC and had a synergistic effect on the process. Peracetylated 2-F-Fuc, a fucosyltransferase activity inhibitor, reduced TSTA3 expression and fucosylation modification of LAMP2 and ERBB2, thereby inhibiting ESCC cell invasion. Conclusion: Our results indicate that TSTA3 may be a driver of ESCC metastasis through regulating fucosylation of LAMP2 and ERBB2. Fucosylation inhibitor may have prospect to suppress ESCC metastasis by blocking aberrant fucosylation.

2.
Acta Biomater ; : 6958, 2020 Sep 29.
Artigo em Inglês | MEDLINE | ID: mdl-33007483

RESUMO

Cation-π interactions play a vital role in modulating various biological processes, e.g., potassium-selective channel, protein folding and adhesion of marine organism. Previous studies mainly focus on binary cation-π interaction, whereas due to the complexity of biological systems and surrounding environments, a single cation is often in close proximity with more than one π-conjugated unit, which could exhibit essentially different binding behavior. Herein, the first experimental evidence of ternary π-cation-π interaction is reported through direct nanomechanical force measurement in a model π-conjugated poly(catechol) (PC) system coexisting with K+. Ternary π-cation-π interactions can bridge π-conjugated moieties, resulting in robust adhesion and promoting PC assembly and deposition. Particularly, these ternary complexes are discovered to transit to binary binding pairs by increasing K+ concentration, undermining adhesion and assembly due to lack of bridging. The π-cation-π binding strength follows the trend of NMe4+ > K+ > Na+ > Li+. Employing the π-cation-π interaction, a deposition strategy to fabricate π-conjugated moiety based adhesive coatings on different substrates is realized. Our findings provide useful insights in engineering wet adhesives and coatings with reversible adhesion properties, and more broadly, with implications on rationalizing biological assembly.

3.
Lipids Health Dis ; 19(1): 217, 2020 Oct 07.
Artigo em Inglês | MEDLINE | ID: mdl-33028331

RESUMO

BACKGROUND: This study explored the relationships between the low-/high-density lipoprotein cholesterol ratio (LDL-C/HDL-C) and other clinical indicators and ischaemic stroke (IS) in patients with non-valvular atrial fibrillation (NVAF) in Xinjiang. The findings could provide a theoretical and therapeutic basis for NVAF patients. METHODS: NVAF patients who were admitted to 10 medical centres across Xinjiang were divided into stroke (798 patients) and control (2671 patients) groups according to the occurrence of first acute IS. Univariate and multivariate logistic regression analysis were used to examine the independent risk factors for IS in NVAF patients. Factor analysis and principal component regression analysis were used to analyse the main factors influencing IS. Receiver operating characteristic (ROC) curve analysis was used to evaluate the discriminatory ability of LDL-C/HDL-C for predicting the occurrence of IS. RESULTS: The stroke group had an average age of 71.64 ± 9.96 years and included 305 females (38.22%). The control group had a mean age of 67.30 ± 12.01 years and included 825 females (30.89%). Multivariate logistic regression showed that the risk of IS in the highest LDL-C/HDL-C quartile (≥2.73) was 16.23-fold that of the lowest quartile (< 1.22); IS risk was 2.27-fold higher in obese patients than in normal-weight subjects; IS risk was 3.15-fold higher in smoking patients than in non-smoking patients. The area under the ROC curve of LDL-C/HDL-C was 0.76, the optimal critical value was 2.33, the sensitivity was 63.53%, and the specificity was 76.34%. Principal component regression analysis showed that LDL-C/HDL-C, age, smoking, drinking, LDL-C and hypertension were risk factors for IS in NVAF patients. CONCLUSIONS: LDL-C/HDL-C > 1.22, smoking, BMI ≥24 kg/m2 and CHA2DS2-VASc score were independent risk factors for IS in NVAF patients; LDL-C/HDL-C was the main risk factor.

4.
Arch Psychiatr Nurs ; 34(5): 394-397, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-33032764

RESUMO

OBJECTIVE: This study aimed to examine the prevalence of sexual harassment (SH) toward Chinese psychiatric nurses and its association with quality of life (QOL). METHODS: A total of 2124 psychiatric nurses were consecutively recruited from 10 psychiatric hospitals distributed across 10 provinces of China; of them, 1,449 were included for analyses. Participants' socio-demographic characteristics, experiences of workplace SH in the past year, and QOL were recorded. RESULTS: Overall, 21.5% (n = 311) of participants reported SH, with 8.4% (n = 121) reporting once, 7.1% (n = 103) reporting twice and 6.0% (n = 87) reporting three times or more. Psychiatric nurses who experienced SH had lower QOL in physical, psychological, social, and environmental domains. Multiple logistic regression analysis found that nurses with shorter clinical experience were more likely to experience SH. CONCLUSIONS: Workplace SH toward psychiatric nurses is common in mental health treatment settings in China. Considering its deleterious impact on nurses' well-being and care quality, effective staff training on the management of SH and a zero tolerance policy against SH should be developed for this population.

5.
Genetica ; 2020 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-33052504

RESUMO

Amphibians are experiencing worldwide declines due to increasing anthropogenetic disturbances. However, the genetic variability and hence adaptability are still unknown for most frogs. We integrated the mitochondrial (ND2 gene), nuclear (TYR gene) and major histocompatibility complex (MHC) loci, to clarify the demographic patterns and immune-gene diversity of the Lolokou Sucker Frog (Amolops loloensis). Demographic analysis of the ND2 and TYR genes suggested that the Lolokou Sucker Frog experienced a population expansion within the last 10,000 years. High MHC diversity was detected, which has likely resulted from positive selection, indicating the current diversity bodes well for the species' adaptive potential to pathogenic challenges. These findings broaden our knowledge on the population history and evolution adaptation of the reclusive torrent frog, and conservation implications are provided.

6.
AJR Am J Roentgenol ; : 1-8, 2020 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-33052737

RESUMO

OBJECTIVE. Deep learning applications in radiology often suffer from overfitting, limiting generalization to external centers. The objective of this study was to develop a high-quality prostate segmentation model capable of maintaining a high degree of performance across multiple independent datasets using transfer learning and data augmentation. MATERIALS AND METHODS. A retrospective cohort of 648 patients who underwent prostate MRI between February 2015 and November 2018 at a single center was used for training and validation. A deep learning approach combining 2D and 3D architecture was used for training, which incorporated transfer learning. A data augmentation strategy was used that was specific to the deformations, intensity, and alterations in image quality seen on radiology images. Five independent datasets, four of which were from outside centers, were used for testing, which was conducted with and without fine-tuning of the original model. The Dice similarity coefficient was used to evaluate model performance. RESULTS. When prostate segmentation models utilizing transfer learning were applied to the internal validation cohort, the mean Dice similarity coefficient was 93.1 for whole prostate and 89.0 for transition zone segmentations. When the models were applied to multiple test set cohorts, the improvement in performance achieved using data augmentation alone was 2.2% for the whole prostate models and 3.0% for the transition zone segmentation models. However, the best test-set results were obtained with models fine-tuned on test center data with mean Dice similarity coefficients of 91.5 for whole prostate segmentation and 89.7 for transition zone segmentation. CONCLUSION. Transfer learning allowed for the development of a high-performing prostate segmentation model, and data augmentation and fine-tuning approaches improved performance of a prostate segmentation model when applied to datasets from external centers.

7.
Phytother Res ; 2020 Oct 02.
Artigo em Inglês | MEDLINE | ID: mdl-33006176

RESUMO

Rheumatoid arthritis (RA) is a chronic autoimmune disease that affects not only joints but also multiple organ systems including cardiovascular system. Endothelial dysfunction plays an important role in cardiovascular diseases (CVD). In RA, endothelial dysfunction exists at both the macrovascular and the microvascular levels, which is a precursor to vasculitis. This study aimed to investigate the pathogenesis of vasculitis and the therapeutic effect of CP-25 on vasculitis in high-fat diet (HFD) collagen-induced arthritis (CIA) rats. Experimental groups were divided into normal group, HFD group, CIA group, HFD CIA group, CP-25 group and MTX group. In vitro, IL-17A was used to stimulate human umbilical vein endothelial cells (HUVECs), and then CP-25 was used to intervene. Results showed that CP-25 reduced global scoring (GS), arthritis index (AI), and swollen joint count (SJC) scores, improved histopathological score, reduced T cells percentage, and decreased IL-17A and ICAM-1 levels. Besides, CP-25 reduced the expression of p-STAT3 to normal levels in vascular of HFD CIA rats. In vitro, IL-17A promoted the expression of p-JAK1, p-JAK2, p-JAK3, pSTAT3, and ICAM-1, and CP-25 inhibited the expression of p-JAK1, p-JAK2, p-JAK3, p-STAT3, and ICAM-1. In conclusion, CP-25 might inhibit endothelial cell activation through inhibiting IL-17A/JAK/STAT3 signaling pathway, which improves vasculitis in HFD CIA rats.

8.
Sci Rep ; 10(1): 16344, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-33004971

RESUMO

Dyslipidemia is one of major risk factors for cardiovascular disease. The early detection and treatment of dyslipidemia can reduce cardiovascular disease risk. A cross-sectional study was carried out in Ningxia, China to determine the prevalence of dyslipidemia and its association with body mass index (BMI) and pubertal stage. A total of 1783 students were selected from middle schools and high schools in September 2014 using stratified random cluster sampling. Serum triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were measured by using MOL-300 automatic biochemical analyzer with associated kits. The prevalence of adolescents with one abnormal serum lipid component was 43.2% and was significantly different across three pubertal stages (p < 0.0001). The abnormal rates of HDL-C and TG increased as the students maturated through the early, middle, and late stages of puberty (all p < 0.0001). Similar results were obtained when separate analyses were performed for boys and girls. In linear regression analysis, BMI was positively associated with serum levels of TC, LDL-C, and TG, but inversely associated with serum levels of HDL-C after the adjustment for age, sex, and race. In multivariable logistic regression analysis, obesity was associated with an increased risk of developing high TC, while pubertal maturation was associated with an elevated risk of experiencing low HDL-C and high TG (all p < 0.05). In conclusions, dyslipidemia is common in an adolescent population of Northwest China and its prevalence rates substantially vary with weight status and pubertal stage.

9.
Mol Cancer Ther ; 2020 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-32999044

RESUMO

Glioma stem cells (GSCs) are essential for tumor maintenance, invasiveness and recurrence. Using a global epigenetic screening with a shRNA library, we identified HDAC3 as essential factor for GSCs stemness. Here we demonstrated GSCs poorly respond to an HDAC3 inhibitor, RGFP966 (HDAC3i), owing to the production of IL-6 and STAT3 activation. To enhance GSCs sensitivity to HDAC3i, we explored if co-treatment with a BRD4 inhibitor, JQ1 (BRD4i) in GSCs produced a better anti-tumor effect. BRD4i synergistically inhibits GSCs growth in association with HDAC3i. HDAC3 inhibition upregulated the acetylation of H3K27 which allowed the recruitment of BRD4 to the GLI1 gene promoter and induced its expression. GLI1, a transcription factor, turned on the expression of IL-6, which led to the activation of STAT3 signaling pathways. However, BRD4i inhibited transcription of GLI1 gene, thereby blocked GLI1/IL-6/STAT3 pathway. In vivo, the HDAC3i/BRD4i combination caused stronger tumor growth suppression than either drug alone. Thus, HDAC3i/BRD4i might provide promising therapies for GBM.

10.
Chin Med J (Engl) ; 2020 Oct 05.
Artigo em Inglês | MEDLINE | ID: mdl-33021767

RESUMO

BACKGROUND: Acute myeloid leukemia (AML) is a malignant hematological disease, originating from hematopoiesis stem cell differentiation obstruction and clonal proliferation. New reagents or biologicals for the treatment of AML are urgently needed, and exosomes have been identified as candidate biomarkers for disease diagnosis and prognosis. This study aimed to investigate the effects of exosomes from bone marrow mesenchymal stem cells (BMSCs) on AML cells as well as the underlying microRNA (miRNA)-mediated mechanisms. METHODS: Exosomes were isolated using a precipitation method, followed by validation using marker protein expression and nanoparticle tracking analysis. Differentially expressed miRNAs were identified by deep RNA sequencing and confirmed by quantitative real-time polymerase chain reaction (qPCR). Cell proliferation was assessed by the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium inner salt method, and cell cycle progression and apoptosis were detected by flow cytometry. Functional gene expression was analyzed by qPCR and Western blotting (WB). Significant differences were determined using Student's t test or analysis of variance. RESULTS: BMSCs-derived exosomes effectively suppressed cell proliferation (both P < 0.0001 at 10 and 20 µg/mL) and cell cycle progression (P < 0.01 at G0-G1 stage), and also significantly enhanced cell apoptosis (P < 0.001) in KG-1a cells. There were 1167 differentially expressed miRNAs obtained from BMSCs-derived exosomes compared with KG-1a cell-derived exosomes (P < 0.05). Knockdown of hsa-miR-124-5p in BMSCs abrogated the effects of BMSCs-derived exosomes in regulating KG-1a such as the change in cell proliferation (both P < 0.0001 vs. normal KG-1a cell [NC] at 48 and 72 h). KG-1a cells treated with BMSCs-derived exosomes suppressed expression of structural maintenance of chromosomes 4 (P < 0.001 vs. NC by qPCR and P < 0.0001 vs. NC by WB), which is associated with the progression of various cancers. This BMSCs-derived exosomes effect was significantly reversed with knockdown of hsa-miR-124-5p (P < 0.0001 vs. NC by WB). CONCLUSIONS: BMSCs-derived exosomes suppress cell proliferation and cycle progression and promote cell apoptosis in KG-1a cells, likely acting through hsa-miR-124-5p. Our study establishes a basis for a BMSCs-derived exosomes-based AML treatment.

11.
Nanotechnology ; 2020 Oct 08.
Artigo em Inglês | MEDLINE | ID: mdl-33032270

RESUMO

Increasing photoactive areas and oxygen vacancy to improve the separation and utilization of electrons and holes in a photocatalytic process are a guarantee for highly photocatalysis efficiency. In this work, we report a CAs@B-TiO2 core-shell nanospheres via a nanoscale water spray assisted method to deposit of black titanium dioxide (B-TiO2) on carbon aerogel sphere (CAs) though slowly hydrolyzing of butyl titanate (e.g. TBOT) in an ethanol-water system. On this basis, furthermore, a facile one-step N2H4·H2O treatment was used to introduces oxygen vacancies on the surface of TiO2 coating layer forming black TiO2. Oxygen vacancies can extend the optical response range of the TiO2 shell from the ultraviolet to the visible region, and increase conductivity and charge transport on the interface of core-shell structure. This study reveals the importance of surface oxygen vacancies for reducing band gaps and developing highly active photocatalysts under visible light.

12.
Oxid Med Cell Longev ; 2020: 5070415, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33014270

RESUMO

Vascular endothelial dysfunction is associated with increased mortality in patients with diabetes. Astragaloside IV (As-IV) is a bioactive saponin with therapeutic potential as an anti-inflammatory and antiendothelial dysfunction. However, the underlying mechanism for how As-IV ameliorated endothelial dysfunction is still unclear. Therefore, in this study, we examined the protective effect of As-IV against endothelial dysfunction and explored potential molecular biology mechanism. In vivo, rats were intraperitoneally injected with streptozotocin (STZ) at a dose of 65 mg/kg body weight to establish a diabetic model. In vitro studies, rat aortic endothelial cells (RAOEC) were pretreated with As-IV, SB203580 (p38 MAPK inhibitor) for 2 h prior to the addition of high glucose (33 mM glucose). Our findings indicated that As-IV improved impaired endothelium-dependent relaxation and increased the levels of endothelial NO synthase (eNOS) and nitric oxide (NO) both in vivo and in vitro. Besides, As-IV treatment inhibited the elevated inflammation and oxidative stress in diabetic model both in vivo and in vitro. Moreover, As-IV administration reversed the upregulated expression of P2X7R and p-p38 MAPK in vivo and in vitro. Additionally, the effects of both P2X7R siRNA and SB203580 on endothelial cells were similar to As-IV. Collectively, our study demonstrated that As-IV rescued endothelial dysfunction induced by high glucose via inhibition of P2X7R dependent p38 MAPK signaling pathway. This provides a theoretical basis for the further study of the vascular endothelial protective effects of As-IV.

13.
Cell Death Dis ; 11(10): 862, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-33060568

RESUMO

As a key enzyme in de novo pyrimidine biosynthesis, the expression level of dihydroorotate dehydrogenase (DHODH) has been reported to be elevated in various types of malignant tumors and its tumor-promoting effect was considered to relate to its pyrimidine synthesis function. Here, we revealed one intriguing potential mechanism that DHODH modulated ß-catenin signaling in esophageal squamous cell carcinoma (ESCC). We demonstrated that DHODH directly bound to the NH2 terminal of ß-catenin, thereby, interrupting the interaction of GSK3ß with ß-catenin and leading to the abrogation of ß-catenin degradation and accumulation of ß-catenin in the nucleus, which in turn, resulted in the activation of ß-catenin downstream genes, including CCND1, E2F3, Nanog, and OCT4. We further demonstrated that the regulation of ß-catenin by DHODH was independent of DHODH catalyzing activity. Univariate and multivariate analyses suggested that DHODH expression might be an independent prognostic factor for ESCC patients. Collectively, our study highlights the pivotal role of DHODH mediated ß-catenin signaling and indicates that DHODH may act as a multi-functional switcher from catalyzing pyrimidine metabolism to regulating tumor-related signaling pathways in ESCC.

14.
Front Immunol ; 11: 558341, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33072096

RESUMO

The host immune system has multiple innate immune receptors that can identify, distinguish and react to viral infections. In innate immune response, the host recognizes pathogen-associated molecular patterns (PAMP) in nucleic acids or viral proteins through pathogen recognition receptors (PRRs), especially toll-like receptors (TLRs) and induces immune cells or infected cells to produce type I Interferons (IFN-I) and pro-inflammatory cytokines, thus when the virus invades the host, innate immunity is the earliest immune mechanism. Besides, cytokine-mediated cell communication is necessary for the proper regulation of immune responses. Therefore, the appropriate activation of innate immunity is necessary for the normal life activities of cells. The suppressor of the cytokine signaling proteins (SOCS) family is one of the main regulators of the innate immune response induced by microbial pathogens. They mainly participate in the negative feedback regulation of cytokine signal transduction through Janus kinase signal transducer and transcriptional activator (JAK/STAT) and other signal pathways. Taken together, this paper reviews the SOCS proteins structures and the function of each domain, as well as the latest knowledge of the role of SOCS proteins in innate immune caused by viral infections and the mechanisms by which SOCS proteins assist viruses to escape host innate immunity. Finally, we discuss potential values of these proteins in future targeted therapies.

15.
Clin Cancer Res ; 2020 Oct 21.
Artigo em Inglês | MEDLINE | ID: mdl-33087333

RESUMO

PURPOSE: We assessed the efficacy and safety of camrelizumab (an anti-PD-1 monoclonal antibody) plus apatinib (a vascular endothelial growth factor [VEGFR]-2 tyrosine kinase inhibitor) in patients with advanced hepatocellular carcinoma (HCC). PATIENTS AND METHODS: This non-randomized, open-label, multicenter, phase 2 study enrolled patients with advanced HCC who were treatment-naive or refractory/intolerant to first-line targeted therapy. Patients received intravenous camrelizumab 200 mg (for bodyweight ≥50 kg) or 3 mg/kg (for bodyweight <50 kg) every 2 weeks plus oral apatinib 250 mg daily. The primary endpoint was objective response rate (ORR) assessed by an independent review committee (IRC) per RECIST v1.1. RESULTS: Seventy patients in the first-line setting and 120 patients in the second-line setting were enrolled. As of January 10, 2020, the ORR was 34.3% (24/70, 95% CI 23.3-46.6) in the first-line and 22.5% (27/120, 95% CI 15.4-31.0) in the second-line cohort per IRC. Median progression-free survival in both cohorts was 5.7 months (95% CI 5.4-7.4) and 5.5 months (95% CI 3.7-5.6), respectively. The 12-month survival rate was 74.7% (95% CI 62.5-83.5) and 68.2% (95% CI 59.0-75.7), respectively. Grade ≥3 treatment-related adverse events (TRAEs) were reported in 147 (77.4%) of 190 patients, with the most common being hypertension (34.2%). Serious TRAEs occurred in 55 (28.9%) patients. Two (1.1%) treatment-related deaths occurred. CONCLUSION: Camrelizumab combined with apatinib showed promising efficacy and manageable safety in patients with advanced HCC in both the first-line and second-line setting. It might represent a novel treatment option for these patients.

16.
Biol Reprod ; 2020 Oct 20.
Artigo em Inglês | MEDLINE | ID: mdl-33079172

RESUMO

Mitophagy is the process by which cells selectively remove supernumerary or damaged mitochondria through autophagy, and is crucial for mitochondrial homeostasis and cell survival. Mitochondria play vital roles in determining the developmental competence of oocytes. During the early stages of oogenesis, aberrant mitochondria can be removed by mitophagy. After oocyte formation, mitophagy is not actively initiated to clear damaged mitochondria despite the presence of mitophagy regulators in oocytes, which leads to the transmission of dysfunctional mitochondria from the oocyte to the embryo. However, granulosa cells around oocytes can improve mitochondrial function through mitophagy, thereby improving oocyte developmental capacity. Furthermore, this review discusses recent work on the substances and environmental conditions that affect mitophagy in oocytes and granulosa cells, thus providing new directions for improving oocyte quality during assisted reproductive technology treatment.

17.
BMC Med Genet ; 21(1): 194, 2020 10 02.
Artigo em Inglês | MEDLINE | ID: mdl-33008326

RESUMO

BACKGROUND: Schizophrenia is a severe, heritable, and refractory psychiatric disorder. Several studies have shown that the disrupted in schizophrenia 1 (DISC1) gene is closely associated with schizophrenia by its role in neuronal morphology, synaptic function, brain development, and dopamine homeostasis etc. This study intended to investigate the expression levels of DISC1 gene in schizophrenia patients compared with healthy controls, and the expression variation of DISC1 gene before and after antipsychotic treatment in schizophrenia patients. METHODS: In this study, we compared DISC1 expression levels in blood of 48 healthy controls, and 32 schizophrenia patients before and after 12 weeks of antipsychotic treatment using real-time quantitative PCR (RT-qPCR) analysis. RESULTS: The expression levels of DISC1 gene in peripheral blood mononuclear cells of schizophrenia patients before antipsychotic treatment were higher than those in healthy controls (P < 0.01); whereas after antipsychotic treatment, the expression levels of DISC1 gene in peripheral blood mononuclear cells of schizophrenia patients still remained increased (P < 0.01). CONCLUSIONS: Our study provided further support for the involvement of DISC1 in the development of schizophrenia.

18.
Eur J Radiol ; 132: 109324, 2020 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-33038576

RESUMO

PURPOSE: Neurocognitive impairment is a common complication in cirrhosis and is associated with alterations in static functional network connectivity (FNC) between distinct brain systems. However, accumulating evidence suggests temporal variability in FNC even at rest. This study aimed to explore dynamic FNC (dFNC) differences and to elucidate their association with neurocognitive changes in cirrhotic patients. METHODS: Fifty-four cirrhotic patients and 42 controls underwent resting-state functional magnetic resonance imaging. Psychometric hepatic encephalopathy score (PHES) was used to assess neurocognitive function. Independent component analysis was performed to identify the components of seven intrinsic brain networks, including sensorimotor (SMN), auditory, visual, cognitive control (CCN), default mode (DMN), subcortical (SC), and cerebellar networks. Sliding window correlation approach was employed to calculate dFNC. FNC states were determined by k-means clustering method, and then functional state analysis was conducted to measure dynamic indices. RESULTS: The patients showed decreased dFNC in State 2, involving the connectivity between posterior subsystem of DMN and CCN (represented by bilateral insular cortex), and in State 3, involving the connectivity between SMN (represented by bilateral precentral gyrus) and SC (represented by bilateral putamen and caudate). The patients spent significantly longer time in State 4 that was with weakest FNC across all networks. We observed a significant correlation between PHES and fraction time/mean dwell time in State 4. CONCLUSIONS: Aberrant dFNC may be the underlying mechanism of neurocognitive impairments in cirrhosis. Dynamic FNC analysis may potentially be utilized in investigating cirrhosis-related neuropathological processes.

19.
Hua Xi Kou Qiang Yi Xue Za Zhi ; 38(5): 513-518, 2020 Oct 01.
Artigo em Chinês | MEDLINE | ID: mdl-33085234

RESUMO

OBJECTIVE: To investigate the expression of glycoprotein 130 (gp130) and interleukin 12 receptor ß2 (IL-12Rß2) in two subunits of interleukin-35 receptor (IL-35R), singal transducer and activator of transcription (STAT) 1 and STAT4 in oral lichen planus (OLP) tissues, and to explore the role and significance of IL-35R in the formation and development of OLP lesions. METHODS: Totally 41 samples of OLP tissues (OLP group) and 15 samples of normal oral mucosa (control group) were collected. The expression levels of gp130, IL-12Rß2, STAT1, STAT4 mRNA in the tissues were detected by real-time fluorescent quantitative polymerase chain reaction and the distribution and expression of protein gp130 and IL-12Rß2 were detected by immunohistochemistry. The potential relationship between gp130 and IL-12Rß2 and clinical features of OLP was analyzed. RESULTS: 1) The expression levels of gp130, IL-12Rß2, STAT1 and STAT4 mRNA in the OLP group were significantly higher than those in the control group (P<0.05). 2) The positive expression rates of gp130 and IL-12Rß2 protein in the OLP group were higher than those in the control group (P<0.05). The expression of gp130 and IL-12Rß2 proteins in OLP tissues were positively correlated (r=0.984, P<0.001). 3) The expression rates of gp130 and IL-12Rß2 protein in erosive OLP tissues were significantly higher than those in non-erosive ones (P<0.05). CONCLUSIONS: The expression of IL-35R and STAT is up-regulated in OLP tissues, and the expression of IL-35R is related to the clinical classification of OLP, suggesting that IL-35R might play an important role in the formation and development of damage OLP lesions.


Assuntos
Líquen Plano Bucal , Humanos , Imuno-Histoquímica , Interleucinas , Mucosa Bucal , RNA Mensageiro
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