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The corrosion of materials severely limits the application scenarios of triboelectric nanogenerators (TENGs), especially in laboratories, chemical plants and other fields where leakage of chemically corrosive solutions is common. Here, we demonstrate a chemical-resistant triboelectric nanogenerator (CR-TENG) based on polysulfonamide (PSA) and polytetrafluoroethylene (PTFE) non-woven fabrics. The CR-TENG can stably harvest biological motion energy and perform intelligent safety protection monitoring in a strong corrosive environment. After treatment with strong acid and alkali solution for 7 days, the fabric morphology, diameter, tensile properties and output of CR-TENG are not affected, showing high reliability. CR-TENG integrated into protective equipment can detect the working status of protective equipment in real time, monitor whether it is damaged, and provide protection for wearers working in high-risk situations. In addition, the nonwoven-based CR-TENG has better wearing comfort and is promising for self-powered sensing in harsh environments.
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Background and aims: The Asian honeybee (Apis cerana) and the European honeybee (Apis mellifera) are reproductively isolated. Previous studies reported that exchanging the larval food between the two species, known as nutritional crossbreeding, resulted in obvious changes in morphology, physiology and behavior. This study explored the molecular mechanisms underlying the honeybee nutritional crossbreeding. Methods: This study used full nutritional crossbreeding technology to rear A. cerana queens by feeding them with an A. mellifera royal jelly-based diet in an incubator. The body color and the expression of certain genes, microRNA, lncRNA, and circRNA among nutritional crossbred A. cerana queens (NQ), and control A. cerana queens (CQ) were compared. The biological functions of two target genes, TPH1 and KMO, were verified using RNA interference. Results: Our results showed that the NQ's body color turned yellow compared to the black control queens. Whole transcriptome sequencing results showed that a total of 1484, 311, 92, and 169 DEGs, DElncRNAs, DEmiRNAs, and DEcircRNAs, respectively, were identified in NQ and CQ, in which seven DEGs were enriched for three key pathways (tryptophan, tyrosine, and dopamine) involved in melanin synthesis. Interestingly, eight DElncRNAs and three DEmiRNAs were enriched into the key pathways regulating the above key DEGs. No circRNAs were enriched into these key pathways. Knocking down two key genes (KMO and TPH1) resulted in altered body color, suggesting that feeding NQ's an RNAi-based diet significantly downregulated the expression of TPH1 and KMO in 4-day-old larvae, which confirmed the function of key DEGs in the regulation of honeybee body color. Conclusion: These findings reveal that the larval diets from A. mellifera could change the body color of A. cerana, perhaps by altering the expression of non-coding RNAs and related key genes. This study serves as a model of epigenetic regulation in insect body color induced by environmental factors.
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Under the limitation of the carrier yield and mobility of semiconductor photocatalysts and the reaction domain, it seems that the photocatalytic efficiency cannot be greatly improved. Here, an efficient contact-electro-catalysis (CEC) system based on droplet triboelectric nanogenerator (TENG) is developed. Instead of using traditional semiconductor catalysts, the electric charge transferred during the electrification process of the contact between water droplets and polytetrafluoroethylene (PTFE) is used to participate in catalysis, and the output electrical signal can also monitor the degree of catalysis. The important role of light in the circulation of this CEC system is studied and discussed for the first time. It is proved that the contact electrification at the liquid-solid interface is accompanied by the generation of a large number of strong oxidizing radicals. The efficient transport of charge carriers driven by mechanical force and the active oxygen species distributed in the whole domain greatly improve the degradation rate of dyes. The experimental data show that the degradation efficiency of crystal violet (CV) reaches 90% within 38 s, and the rate constant k is as high as 3.7 min-1. This is a breakthrough in the field of catalysis.
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BACKGROUND: The role of HER2 overexpression in rectal cancer is controversial. AIM: To assess the role of HER2 overexpression in the long-term prognosis of rectal cancer. METHODS: Data from patients with locally advanced rectal cancer who underwent total mesorectal excision after short-course radiotherapy at Beijing Cancer Hospital between May 2002 and October 2005 were collected. A total of 151 tissue samples of rectal cancer were obtained using rigid proctoscopy before neoadjuvant radiotherapy, followed by immunohistochemistry and fluorescence in situ hybridisation to determine the patients' HER2 expression status. Univariate and multivariate analyses of the associations between the clinicopathological factors and HER2 status were performed. Survival was estimated and compared using the Kaplan-Meier method based on HER2 expression status, and the differences between groups were verified using the log-rank test. RESULTS: A total of 151 patients were enrolled in this study. A total of 27 (17.9%) patients were ultimately confirmed to be HER2-positive. The follow-up duration ranged from 9 mo to 210 mo, with a median of 134 mo. Distant metastasis and local recurrence occurred in 60 (39.7%) and 24 (15.9%) patients, respectively. HER2 positivity was significantly associated with the pre-treatment lymph node stage (pre-N) (P = 0.040), while there were no differences between HER2 status and age, sex, preoperative CEA levels (pre-CEA), T stage, and lympho-vascular invasion. In terms of prognosis, HER2 overexpression was correlated with distant metastasis (P = 0.002) rather than local recurrence (P > 0.05). The multivariate analysis demonstrated that elevated pre-CEA [P = 0.002, odds ratio (OR) = 3.277, 97.5% confidence interval (CI): 1.543-7.163], post N(+) (P = 0.022, OR = 2.437, 97.5%CI: 1.143-5.308) and HER2(+) (P = 0.003, OR = 4.222, 97.5%CI: 1.667-11.409) were risk factors for distant metastasis. The survival analysis showed that there were significant differences between rectal cancer patients in terms of disease-free survival (DFS) [hazard ratio: 1.69 (95%CI: 0.91-3.14); P = 0.048] and overall survival (OS) [1.95 (1.05-3.63); P = 0.0077]. CONCLUSION: HER2 overexpression is a potential biomarker for predicting lymph node metastasis and distant metastasis, which are associated with worse long-term DFS and OS in rectal cancer patients with locally advanced disease.
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This article focuses on engineering Corynebacterium glutamicum to produce L-lysine efficiently from starch using combined method of "classical breeding" and "genome breeding." Firstly, a thermo-tolerable L-lysine-producing C. glutamicum strain KT45-6 was obtained after multi-round of acclimatization at high temperature. Then, amylolytic enzymes were introduced into strain KT45-6, and the resultant strains could use starch for cell growth and L-lysine production except the strain with expression of isoamylase. In addition, co-expression of amylolytic enzymes showed a good performance in starch degradation, cell growth and L-lysine production, especially co-expression of α-amylase (AA) and glucoamylase (GA). Moreover, L-lysine yield was increased by introducing AA-GA fusion protein (i.e., strain KT45-6S-5), and finally reached to 23.9 ± 2.3 g/L in CgXIIIPM-medium. It is the first report of an engineered L-lysine-producing strain with maximum starch utilization that may be used as workhorse for producing amino acid using starch as the main feedstock. KEY POINTS: ⢠Thermo-tolerable C. glutamicum was obtained by temperature-induced adaptive evolution. ⢠The fusion order between AA and GA affects the utilization efficiency of starch. ⢠C. glutamicum with starch utilization was constructed by optimizing amylases expression.
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Corynebacterium glutamicum , Corynebacterium glutamicum/genética , Corynebacterium glutamicum/metabolismo , Fermentación , Lisina/metabolismo , Ingeniería Metabólica , Almidón/metabolismo , Zea mays/metabolismoRESUMEN
Stress response is an adaptive process of the organism to confront environmental perturbation. Moderate stress response induces the organism to establish effective adaptive strategies for survival, while excessive stress response results in stress injury, which is a major cause of a variety of physical or psychological diseases, including diabetes mellitus. Diabetes mellitus is a typical stress-related disease, with numerous evidence indicating that the development and progression of diabetes mellitus are closely related to stress response, such as metabolic stress, oxidative stress and endoplasmic reticulum stress. However, the detailed mechanisms of stress response mediated regulation of diabetes mellitus and how to prevent or treat diabetes mellitus via modification of stress response remain to be further investigated. Here, we will introduce the definition and regulatory mechanisms of stress response, as well as discuss the biological functions and mechanisms of various stress responses during the pathogenesis of diabetes mellitus. This review highlights recent advances of stress medicine associated with diabetes mellitus, in order to provide theoretical basis and reference for prevention and treatment of diabetes mellitus. Future studies should focus on elucidating the clinical application potential of the key factors of stress response that mediate the pathogenesis of diabetes mellitus, as well as boosting the related translational medicine studies.
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Diabetes Mellitus , Diabetes Mellitus/etiología , Estrés del Retículo Endoplásmico , Humanos , Estrés OxidativoRESUMEN
OBJECTIVE: We aim to investigate the anticancer effects and mechanisms of icaritin against breast cancer. MATERIALS AND METHODS: Both estrogen receptor (ER) positive breast cancer cells MCF- 7 and ER-negative MDA-MB-231 cells were employed. We examined the effects of icaritin on the proliferation and migration by wound healing assay and transwell assay. Cell apoptosis and cell cycle of MCF-7 and MDA-MB-231 cells were analyzed using Flow cytometry. Cell autophagy of MCF-7 and MDA-MB-231 cells was assessed by western blotting, acridine orange staining and confocal microscopy. We also detected the expression of apoptosis-related genes by western blotting. In addition, an autophagy inhibitor was used to investigate whether cytoprotective autophagy was induced. Meanwhile, an ER inhibitor was utilized to explore whether ER was involved in autophagy. RESULTS: Icaritin inhibited the proliferation and migration, and induced cell cycle arrest of both MDA-MB-231 and MCF-7 cells. Icaritin significantly induced apoptosis of MDA-MB- 231 cells by activating caspase-3. And icaritin stimulated autophagy in MCF-7 cells, as evidenced by increased LC3II/LC3I, enhanced p62 degradation, the accumulation of endogenous LC3 puncta formation, and the increased autophagy flux. Icaritin induced autophagy through upregulating the phosphorylation of AMPK and ULK1. Chloroquine, an autophagy inhibitor, increased icaritin-induced apoptosis and proliferation inhibition of MCF-7 cells. Meanwhile, tamoxifen, an ER inhibitor, reversed icaritin-induced autophagy and proliferation inhibition of MCF-7 cells. CONCLUSION: Our study demonstrated that the antitumor effects of icaritin against breast cancer are related to ER, which suggested that the status of ER should be considered in the clinical application of icaritin.
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Autofagia , Neoplasias de la Mama/tratamiento farmacológico , Flavonoides/farmacología , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Receptores de Estrógenos/metabolismo , Apoptosis , Proteínas Reguladoras de la Apoptosis/genética , Proteínas Reguladoras de la Apoptosis/metabolismo , Neoplasias de la Mama/genética , Neoplasias de la Mama/metabolismo , Neoplasias de la Mama/patología , Ciclo Celular , Proliferación Celular , Femenino , Humanos , Receptores de Estrógenos/genética , Transducción de Señal , Células Tumorales CultivadasRESUMEN
OBJECTIVE: Hepatic portal pneumatosis has a high mortality rate, and whether surgical intervention is necessary remains controversial. This experiment retrospectively analyzed the etiology, treatment methods and prognosis of adult patients with hepatoportal pneumocele to provide a theoretical basis for the treatment of this disease. METHODS: We analyzed the clinical symptoms and post-treatment of a 43-year-old male patient with HPVG admitted to hospital. We retrieved adult non-iatrogenic HPVG cases with complete clinical data in PUBMED, and MEDLINE and other databases were retrieved for analysis, and summarized the pathogenesis, clinical symptoms, pathogenesis, pathogenesis and prognosis of different treatment schemes were summarized. RESULTS: The main etiology of HPVG are intestinal ischemia (27%), severe enteritis/intestinal perforation/intestinal fistula (16%), intestinal obstruction (7%), abdominal infection (7%), gastric diseases (11%), appendicitis and its complications (5%), acute hemorrhage or necrotizing pancreatitis (5%), Crohn's disease and its complications (4%), trauma (traffic accidents, falls) (2%), diverticulitis and perforation (6%), nephrogenic diseases (4%), spontaneous pneumohepatic portal vein (2%), other reasons (4%). And after analysis, we found that the survival rate of patients treated by surgery was 40.5% and the mortality rate was 19.1%, the difference between the two was significant. CONCLUSIONS: Etiology should be actively explored and surgical treatment is necessary.
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Embolia Aérea/diagnóstico , Vena Porta/patología , Adulto , Embolia Aérea/etiología , Resultado Fatal , Venas Hepáticas/diagnóstico por imagen , Venas Hepáticas/patología , Humanos , Masculino , Venas Mesentéricas/diagnóstico por imagen , Venas Mesentéricas/patología , Vena Porta/diagnóstico por imagen , Choque Séptico/complicaciones , Tomografía Computarizada por Rayos XRESUMEN
Background: Lung ischemia reperfusion injury (LIRI) is a complex pathophysiological process activated by lung transplantation and acute lung injury. The p38 mitogen-activated protein kinase (MAPK) is involved in breakdown of the endothelial barrier during LIRI, but the mechanism is still unclear. Therefore, we investigated the function of p38 MAPK in LIRI in vivo and in vitro. Methods: Sprague-Dawley rats were subjected to ischemia reperfusion with or without pretreatment with a p38 MAPK inhibitor. Lung injury was assessed using hematoxylin and eosin staining, and pulmonary blood-air barrier permeability was evaluated using Evans blue staining. A rat pulmonary microvascular endothelial cell line was infected with lentiviral expressing short hairpin (sh)RNA targeting p38 MAPK and then cells were subjected to oxygen/glucose deprivation and reoxygenation (OGD/R). Markers of endothelial destruction were measured by western blot and immunofluorescence. Results: In vivo LIRI models showed structural changes indicative of lung injury and hyperpermeability of the blood-air barrier. Inhibiting p38 MAPK mitigated these effects. Oxygen/glucose deprivation and reoxygenation promoted hyperpermeability of the endothelial barrier in vitro, but knockdown of p38 MAPK attenuated cell injury; maintained endothelial barrier integrity; and partially reversed injury-induced downregulation of permeability protein AQP1, endothelial protective protein eNOS, and junction proteins ZO-1 and VE-cadherin while downregulating ICAM-1, a protein involved in destroying the endothelial barrier, and ET-1, a protein involved in endothelial dysfunction. Conclusion: Inhibition of p38 MAPK alleviates LIRI by decreasing blood-air hyperpermeability. Blocking p38 MAPK may be an effective treatment against acute lung injury.
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BACKGROUND: Plasmid construction of small fragments of interest (such as insertion of small fragment marker genes, expression of shRNA, siRNA, etc) is the basis of many biomolecular experiments. Here, we describe a method to clone short DNA into vectors by polymerase chain reaction (PCR), named one-step PCR cloning. Our method uses PCR to amplify the entire circular plasmid. The PCR was performed by the primers containing the gene of short DNA with overlapping sequences between 10-15 bp. The PCR products were then transformed into E. coli and cyclized by homologous recombination in vivo. METHODS: The pEGFP-N1-HA plasmid was constructed by one-step PCR and transformation. Cells were transfected with pEGFP-N1-HA and pEGFP-N1 plasmid using TurboFect transfection reagent. Protein expression was detected by western blotting and the HA-GFP fusion protein was detected by confocal microscopy. RESULTS: The pEGFP-N1-HA plasmid was successfully constructed and HA expression in cells. CONCLUSIONS: Free from the limitations of restriction enzyme sites and omitting the ligation process, our method offers a flexible and economical option of plasmid construction. KEY POINTS: Significant findings of the study A method to clone short DNA into plasmids was found. What this study adds Our study provides a flexible and economical option to clone short DNA into plasmids.
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Clonación Molecular/métodos , ADN/metabolismo , Plásmidos/metabolismo , Reacción en Cadena de la Polimerasa/métodos , HumanosRESUMEN
BACKGROUND: Microparticles (MPs) are small extracellular plasma membrane particles shed by activated and apoptotic cells, which are involved in the development of atherosclerosis. Our previous study found that microRNA (miR)-19b encapsulated within endothelial MPs (EMPs) may contribute to the upregulation of circulating miR-19b in unstable angina patients. Hypoxia is involved in atherosclerosis as a critical pathological stimulus. However, it still remains unclear whether the increase of miR-19b levels in EMPs is related to hypoxia and if the effect of miR-19b - wrapped within EMPs - stimulates hypoxia on vascular endothelial cells. This study aimed to explore the changes of miR-19b in EMPs induced by hypoxia as well as their effects on endothelial cells. METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured in vitro and arranged to harvest EMPs in two parts: the first part consisted of EMPcontrol and EMPhypoxia and the second part included EMPvehicle, EMPNC mimic, and EMPmiR-19b mimic. Cell migration was detected by scratch migration and transwell chamber migration. Angiogenesis was assessed by tube formation assays. Furthermore, we predicted the target gene of miR-19b by bioinformatics analysis, and luciferase assay was used to verify the targeted gene of miR-19b. Data were analyzed by one-way analysis of variance. Student's t-test was used when two groups were compared. RESULTS: Compared with EMPcontrol- and EMPhypoxia-inhibited migration of cells by scratch migration assay (80.77 ± 1.10 vs. 28.37 ± 1.40, P < 0. 001) and transwell chamber migration assay (83.00 ± 3.46 vs. 235.00 ± 16.52, P < 0.01), the number of tube formations was markedly reduced by 70% in the EMPhypoxia group (P < 0.001) in vitro analysis of HUVECs. Meanwhile, a strong inhibition of migration and tube formation of HUVECs in the presence of miR-19b-enriched EMPmiR-19b mimic was observed. This effect might be due to the delivery of miR-19b in EMPs. Transforming growth factor-ß2 (TGFß2) was predicted to be one of the target genes of miR-19b, and we further confirmed that TGFß2 was a direct target gene of miR-19b using the luciferase assay. The expression of TGFß2 in HUVECs was inhibited by treatment with EMPhypoxia and EMPmiR-19b mimic. CONCLUSIONS: MiR-19b in EMPs induced by hypoxia could reduce endothelial cell migration and angiogenesis by downregulating TGFß2 expression, which may have inhibited the progression of atherosclerosis.
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Células Endoteliales/metabolismo , Células Endoteliales de la Vena Umbilical Humana/metabolismo , MicroARNs/metabolismo , Hipoxia de la Célula/genética , Hipoxia de la Célula/fisiología , Movimiento Celular/genética , Movimiento Celular/fisiología , Humanos , MicroARNs/genética , Neovascularización Fisiológica/genética , Neovascularización Fisiológica/fisiología , Factor de Crecimiento Transformador beta2/genética , Factor de Crecimiento Transformador beta2/metabolismoRESUMEN
OBJECTIVE: To investigate the expression of mRNA of aspartyl/asparaginyl beta-hydroxylase (ASPH) gene in invasive breast cancer (IBC) and the relationship between methylation of gene promoter and clinicopathological parameters. METHODS: In 91 cases of breast cancer tissues and matched normal tissues (MNT),mRNA expression of the ASPH gene was detected by reverse transcription of real-time fluorescence quantification PCR and the methylation status of CpG island in the ASPH gene promoter region was detected by methylation specific PCR (MSP).And the relationship between the expression and the clinicopathological features of breast cancer was analyzed. RESULTS: The expression of ASPH gene mRNA in IBC was significantly higher than that in MNT ( P<0.001).The fold change of ASPH mRNA expression was related to whether E-cadherin was positive (r=0.195, P=0.041).The positive rate of methylation of ASPH gene promoter in breast cancer and MNT was 47.3% (43/91) and 89.0% (81/91). The methylation rate of gene promoter was correlated with E-cadherin and tumor size ( P<0.05). CONCLUSION: The mRNA expression and promoter methylation rate of ASPH gene may play a role in the development and progression of breast cancer.
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Neoplasias de la Mama/genética , Proteínas de Unión al Calcio/genética , Metilación de ADN , Proteínas de la Membrana/genética , Oxigenasas de Función Mixta/genética , Proteínas Musculares/genética , Regiones Promotoras Genéticas , Antígenos CD/metabolismo , Cadherinas/metabolismo , Estudios de Casos y Controles , Islas de CpG , Regulación Neoplásica de la Expresión Génica , Humanos , ARN MensajeroRESUMEN
There is limited knowledge regarding the influence of autophagy on the anticancer effect of dihydroartemisinin (DHA). The present study aimed to investigate this influence within human breast cancer cells. Changes in cell viability, cell cycle distribution, apoptosis and associated genes were analyzed in MDA-MB-231 cells subjected to DHA following alteration in autophagy levels; the autophagy level was decreased following autophagy-related 7 (Atg7) knockdown or increased using rapamycin. The data indicated that rapamycin had the ability to notably enhance the anticancer effect of DHA on MDA-MB-231 cells. Autophagy induction may be key in mediating the anticancer effects of DHA, and rapamycin may regulate the death-associated protein kinase via the alteration of Atg7 expression, which would influence cell apoptosis. The present study presented a novel insight into enhancing the effectiveness of future treatment regimens for breast cancer using DHA.
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BACKGROUND: In the previous study, we established an ischemia-prone gerbil population (IG), which was selectively bred to increase the incidence of unilateral carotid arterial occlusion (UCO)-induced ischemia in Mongolian gerbils. However, if the characteristics of ischemia model in IG are the same as those in general gerbils (GG), and if the neurological symptoms are associated with the neurological insults in IG is still unclear. METHODS: In the present study, we evaluated the UCO model in IG by analyzing neurological symptoms, neurological injury in the hippocampal CA1 region and compared with GG. RESULTS: The data showed that the ratios of neurological symptom scores ≥ 2 in the IG and GG groups were 65.0% vs 30.0%, respectively, and were significantly different (P < .01).The neuronal damage following a UCO ischemic insult in the IG group was more severe compared to the GG group. There was a high correlation between the neurological insults' scale and the neurological symptom score in the IG and GG groups (r = .979 and .943 in the IG and GG groups, respectively). In animals with mild neurological symptom scores (2 and 3), the neuronal insults were significantly different between female and male gerbils in both IG and GG. CONCLUSION: Our findings suggest that IG population would likely be more advantageous to establish an ischemic model.
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The complete mitochondrial genome of the Tamarisk jird, Meriones tamariscinus, was sequenced. The 16,389bp genome contains 37 genes, typical for rodent mitogenomes, including 22 tRNA genes, 2 rRNA genes, and 13 protein-coding genes. The total GC content of the mitochondrial genome is 36.8%, with a base composition of 34.0% A, 24.5% C, 12.3% G, and 29.2% T. The phylogenetic analysis showed that M. tamariscinus was classified in the genus Meriones, Muridae.
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This study investigates the sensitivity of a three-dimensional (3D) indoor ray tracing (RT) model for the use of the uniform theory of diffraction and geometrical optics in radio channel characterizations of indoor environments. Under complex indoor environments, RT-based predictions require detailed and accurate databases of indoor object layouts and the electrical characteristics of such environments. The aim of this study is to assist in selecting the appropriate level of accuracy required in indoor databases to achieve good trade-offs between database costs and prediction accuracy. This study focuses on the effects of errors in indoor environments on prediction results. In studying the effects of inaccuracies in geometry information (indoor object layout) on power coverage prediction, two types of artificial erroneous indoor maps are used. Moreover, a systematic analysis is performed by comparing the predictions with erroneous indoor maps and those with the original indoor map. Subsequently, the influence of random errors on RMS delay spread results is investigated. Given the effect of electrical parameters on the accuracy of the predicted results of the 3D RT model, the relative permittivity and conductivity of different fractions of an indoor environment are set with different values. Five types of computer simulations are considered, and for each type, the received power and RMS delay spread under the same circumstances are simulated with the RT model.
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Epigenetic modifications are critical determinants in tumor initiation and progression. This study aims to detect the promoter methylation status and the mRNA expression levels of ATG2B, ATG4D, ATG9A and ATG9B, and then to explore their relationship in invasive ductal carcinomas (IDCs) and matched normal tissues (MNTs) of the breast. Methylation was observed as follows: 61.0% in ATG2B, 46.8% in ATG4D, 56.4% in ATG9A, and 74.0% in ATG9B of IDCs. Meanwhile, their mRNA expression levels of the IDCs was lower than that of the MNTs (P<0.001, P=0.019, P<0.001 and P<0.001, respectively). Methylated IDCs of ATG2B, ATG9A, ATG9B and unmethylated ATG4D, ATG9B showed significantly lower expression values compared to the MNTs (P=0.003, P<0.001, P<0.001, P=0.014 and P=0.002, respectively). The methylations of ATG2B and ATG9B were related to their lower expression levels in IDCs (P=0.017 and P=0.023). Moreover, ATG2B methylation was positively associated with the grade (P=0.024) and TNM stage (P=0.015); Methylation of ATG4D and ATG9A was positively correlated to lymph node involvement (P=0.012 and P=0.018), while methylation of ATG9B appeared susceptible to CK5/6 positive status and deteriorated TNM stages (P=0.003 and P=0.012). Moreover, the decreased expression of ATG2B was related to the ER and PR status (P=0.004 and P=0.003). The ER, HER-2 and lymph node metastasis status are the determinants to reducing the expression of ATG4D, ATG9A and ATG9B (P=0.026, P=0.010 and P=0.011, respectively). This study highlights the transcriptional inactivation mechanisms of ATG2B, ATG4D, ATG9A and ATG9B promoter methylation status and the possible origin of autophagy signal pathway repression in IDCs.
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Proteínas Relacionadas con la Autofagia/genética , Neoplasias de la Mama/genética , Islas de CpG/genética , Metilación de ADN/genética , Regulación Neoplásica de la Expresión Génica , Regiones Promotoras Genéticas , Proteínas Relacionadas con la Autofagia/metabolismo , Neoplasias de la Mama/patología , Carcinoma Ductal de Mama/genética , Carcinoma Ductal de Mama/patología , Cisteína Endopeptidasas/genética , Cisteína Endopeptidasas/metabolismo , Femenino , Humanos , Proteínas de la Membrana/genética , Proteínas de la Membrana/metabolismo , ARN Mensajero/genética , ARN Mensajero/metabolismo , Proteínas de Transporte Vesicular/genética , Proteínas de Transporte Vesicular/metabolismoRESUMEN
OBJECTIVE: To investigate the expressions and clinical significance of autophagy-related gene 2B (ATG2B), autophagy-related gene 4D (ATG4D), autophagy-related gene 9B (ATG9B) in breast cancer cell lines and breast cancer. METHODS: Cancer Browser screening was applied to study the differential expressions of ATG2B, ATG4D, ATG9B genes in breast cancer. Quantitative Real-time PCR was used to measure the expressions of these three genes in human breast cancer cell lines (MCF-7, MDA-MB-231, MDA-MB-435S and ZR-75-30) as well as 83 cases of breast cancer samples with paired normal breast tissues. The relationships between the expressions of these genes and clinicopathological characteristics were further analyzed. RESULTS: Cancer Browser screening found abnormal expressions of ATG2B, ATG4D, ATG9B in breast cancer (P = 0.015, P = 0.028, P = 0.040). All four breast cancer cell lines expressed ATG2B, ATG4D, ATG9B, and the expression of ATG2B, ATG9B was significantly lower than positive control (P < 0.001), but ATG4D expression was higher than positive control (P < 0.001). The expressions of ATG2B, ATG4D, ATG9B in breast cancer were all lower than those in the adjacent normal tissues (P < 0.001, P = 0.031, P < 0.001). Furthermore, the expression of ATG2B was correlated with ER (r = 0.949, P = 0.015), and the expression of ATG4D was related to age (r = -0.449, P = 0.005), the expression of ATG9B was correlated to lymph node metastasis and cytokeratin 5/6 status (r = 0.339, P = 0.043; r = 0.533, P = 0.043). CONCLUSION: ATG2B, ATG4D, ATG9B genes shows low expressions in breast cancer, which may become new molecular markers for the prognosis of breast cancer.
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Autofagia , Neoplasias de la Mama/genética , Cisteína Endopeptidasas/genética , Proteínas de la Membrana/genética , Proteínas de Transporte Vesicular/genética , Proteínas Relacionadas con la Autofagia , Línea Celular Tumoral , Femenino , Humanos , Metástasis Linfática , PronósticoRESUMEN
In the last decade, the overexpression of hepatoma upregulated protein (HURP) has been reported in hepatocellular carcinoma, adrenocortical tumors and urogenital carcinoma. However, the role of HURP in breast cancer remains unknown. In the present study, a comprehensive analysis was performed to examine the HURP expression level in 43 breast cancer tumor samples and paired adjacent normal tissues. The correlation between the HURP expression level and the clinicopathological characteristics was evaluated. The role of HURP in breast cancer was investigated by quantitative polymerase chain reaction, western blot analysis and cell proliferation assays. HURP expression was found to be significantly increased in the breast cancer samples. The HURP expression level was higher in the tumors with advanced-grade metastasis and was strongly associated with tumor-node-metastasis staging (P=0.003). Transfection and cell proliferation assays suggested that the suppression of HURP expression or the interference in HURP activity in the breast cancer cells inhibited cell proliferation significantly. These data suggest that HURP is associated with the degree of malignancy and the proliferation of breast cancer. HURP could be a tumor biomarker for prognosis and a potential therapeutic drug target for human breast cancer.
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In order to estimate the sparse vegetation information accurately in desertification region, taking southeast of Sunite Right Banner, Inner Mongolia, as the test site and Tiangong-1 hyperspectral image as the main data, sparse vegetation coverage and biomass were retrieved based on normalized difference vegetation index (NDVI) and soil adjusted vegetation index (SAVI), combined with the field investigation data. Then the advantages and disadvantages between them were compared. Firstly, the correlation between vegetation indexes and vegetation coverage under different bands combination was analyzed, as well as the biomass. Secondly, the best bands combination was determined when the maximum correlation coefficient turned up between vegetation indexes (VI) and vegetation parameters. It showed that the maximum correlation coefficient between vegetation parameters and NDVI could reach as high as 0.7, while that of SAVI could nearly reach 0.8. The center wavelength of red band in the best bands combination for NDVI was 630nm, and that of the near infrared (NIR) band was 910 nm. Whereas, when the center wavelength was 620 and 920 nm respectively, they were the best combination for SAVI. Finally, the linear regression models were established to retrieve vegetation coverage and biomass based on Tiangong-1 VIs. R2 of all models was more than 0.5, while that of the model based on SAVI was higher than that based on NDVI, especially, the R2 of vegetation coverage retrieve model based on SAVI was as high as 0.59. By intersection validation, the standard errors RMSE based on SAVI models were lower than that of the model based on NDVI. The results showed that the abundant spectral information of Tiangong-1 hyperspectral image can reflect the actual vegetaion condition effectively, and SAVI can estimate the sparse vegetation information more accurately than NDVI in desertification region.