Αρχειοθήκη ιστολογίου

Πέμπτη 1 Απριλίου 2021

Sphenoid Sinus: Pneumatization and Septation Patterns in a Hispanic Population

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Introduction: Pneumatization of the sphenoid sinus (SS) varies widely among different ethnic groups. Information regarding the prevalence and significance of SS variants among Hispanic groups is limited. This study aims to describe and analyze pneumatization and septation patterns of the SS in a Hispanic population. Methods: A total of 160 paranasal sinus computed tomographies were reviewed by a head and neck-specialized radiologist and 2 otolaryngologists. R esults: The postsellar and sellar types were the most frequent patterns of pneumatization observed, with a prevalence of 52.5 and 40%, respectively. Accessory septations were present in 59.4% of the patients. Septa were inserting over the internal carotid artery (ICA) in 43.8% and over the optic nerve in 17.5% of the population. No significant association (p #x3e; 0.05) was observed when comparing the different accessory septation patterns among the types of the SS. The frequency of septa inserting on the ICA was significantly higher in postsellar types (p #x3c; 0.001). Pneumatization of the anterior clinoid process, pterygoid processes, and greater wing was present in 20, 17.5, and 45.9% of the sinuses, respectively. Onodi cells were encountered in 40% of the sinuses. There were no significant differences in any of the pneumatization and septation variables when compared by gender and age (p #x3e; 0.05). Discussion/Conclusion: Differences regarding anatomical variants and septations of the SS were observed in our study when compared with findings reported in other ethnic groups. Preoperative assessment of the anatomical variants of the SS in Mexican patients is imperative to select the most optimal surgical approach and prevent iatrogenic injuries to related neurovascular structures.
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Pragmatic Skills in Children with Hearing Loss: Comparison Between Cochlear Implants and Hearing Aids Users

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Abstract

Pragmatic language ability denotes the ability to use language in a social context. There is a lack of research that has compared children's pragmatic skills with hearing loss with those of hearing peers. This study questioned whether children with a cochlear implant would show better pragmatic skills than children with hearing aids. 52 children were included in three groups: cochlear implant (n = 16), hearing aid (n = 16), and normal hearing (n = 20). The participants' pragmatic skills were evaluated using the Persian version of the children's communication checklist. Of the 52 participants recruited, 22 (42.3%) were males, and 30 (57.7%) were females. The mean age of the CI, HA, and NH group participants was 75.19 ± 10.80, 72.19 ± 8.68, and 68.90 ± 6.78 months, respectively (P > 0.05). There was a significant difference between the mean scores of Speech Output and Syntax between the groups (CI, HA and NH) (P < 0.001). The hearing-impaired children show acceptable pragmatic skills in comparison with NH children. Specialists, such as teachers and clinicians, should be alert of the abilities and difficulties that the hearing-impaired children might be facing in the regular classroom.

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Novel PRRT2 gene variants identified in paroxysmal kinesigenic dyskinesia and benign familial infantile epilepsy in Chinese families

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Exp Ther Med. 2021 May;21(5):504. doi: 10.3892/etm.2021.9935. Epub 2021 Mar 18.

ABSTRACT

The present study was performed to investigate the clinical manifestations and pathogenic variants in three large families with autosomal dominant paroxysmal kinesigenic dyskinesia (PKD) and/or benign familial infantile epilepsy (BFIE) in China. Detailed clinical data and family history were collected. Genomic DNA was isolated from the peripheral blood samples of all available members. The genetic diagnosis was made by whole-exome sequencing on the three probands and the candidate variants were verified by PCR-Sanger sequencing. The pathogenicity of variants was predicted by bioinformatics analyses and classified according to the American College of Medical Genetics criteria. A total of three causative heterozygous variants were identified in the proline-rich transmembrane protein 2 (PRRT2) gene by DNA sequencing: A novel c.324_334del(p.Val109Argfs *21) deletion variant in Family A, as well as the previously known c.510_513del(p.Ser172Argfs*3) deletion variant in Family B and c.649dupC(p.Arg217Profs*8) duplication variant in Family C. The three variants of PRRT2 co-segregated with the phenotype and genotype in the family members. The present results deepen the current understanding of PKD/BFIE and extend the genotypic-phenotypic spectrum of PKD/BFIE.

PMID:33791013 | PMC:PMC8005681 | DOI:< a href="https://doi.org/10.3892/etm.2021.9935" target="_blank" rel="noopener" class="underlink bluelink" tabindex="-1">10.3892/etm.2021.9935

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Effects of lumican expression on the apoptosis of scleral fibroblasts: In vivo and in vitro experiments

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Exp Ther Med. 2021 May;21(5):495. doi: 10.3892/etm.2021.9926. Epub 2021 Mar 17.

ABSTRACT

Lumican serves an important role in the maintenance of sclera biomechanical properties. However, whether lumican expression is altered in myopia and the mechanisms of action involved are unknown. In the present study, the expression of lumican in cultured scleral fibroblasts and in the scleral tissue of a rat model of form-deprivation myopia was assessed. It was confirmed that diopter was decreased, whereas axial length was increased in modeled eyes relative to normal control eyes, indicating that the model of myopia was successfully established. These pathologic changes were accompanied by the upregulation of lumican and tissue inhibitor of metalloproteinases (TIMP)-2, as well as the downregulation of matrix metalloproteinase (MMP)-2 and MMP-14. The same trends in TIMP-2, MMP-2 and MMP-14 expression were observed when lumican was overexpressed in cultured scleral fibroblasts. Additionally, cell proliferation decreased whereas apoptosis increased compared with those of control cells. Inhibiting lumican expression had no effect on cell proliferation or apoptosis, but stimulated the expression of MMP-2 and MMP-14 while decreasing that of TIMP-2. The results suggested that lumican overexpression contributed to myopia by promoting apoptosis in scleral fibroblasts via the modulation of TIMP-2, MMP-2 and MMP-14 expression.

PMID:33791004 | PMC:PMC8005674 | DOI:10.3892/etm.2021.9926

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Critical roles of Rad54 in tolerance to apigenin-induced Top1-mediated DNA damage

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Exp Ther Med. 2021 May;21(5):505. doi: 10.3892/etm.2021.9936. Epub 2021 Mar 18.

ABSTRACT

Apigenin (APG), a flavone sub-class of flavonoids, possesses a diverse range of biological activities, including anti-cancer and anti-inflammatory effects. Previous studies identified the genotoxicity of APG in certain cancer cells, which may be associated with its anticancer effect. However, the DNA damage repair mechanism induced by APG has remained elusive. In order to clarify the molecular mechanisms, the present study determined the toxicity of APG to the wild-type (WT) DT40 chicken B-lymphocyte cell line, as well as to DT40 cells with deletions in various DNA repair genes, and their sensitivities were compared. It was demonstrated that cells deficient of Rad54, a critical homologous recombination gene, were particularly sensitive to APG. Cell-cycle analysis demonstrated that APG caused an increase in the G2/M-phase populatio n of Rad54- / - cells that was greater than that in WT cells. Furthermore, it was demonstrated by immunofluorescence assay that Rad54- / - cells exhibited significantly increased numbers of γ-phosphorylated H2AX variant histone foci and chromosomal aberrations compared to the WT cells in response to APG. Of note, the in vitro complex of enzyme assay indicated that APG induced increased topoisomerase I (Top1) covalent protein DNA complex in Rad54- / - cells compared to WT cells. Finally, these results were verified using the TK6 human lymphoblastoid cell line and it was demonstrated that, as for DT40 cells, Rad54 deficiency sensitized TK6 cells to APG. The present study demonstrated that Rad54 was involved in the repair of APG-induced DNA damage, which was associated with Top1 inhibition.

PMID:33791014 | PMC:PMC8005727 | DOI:10.3892/etm.2021.9936

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Knockdown of lncRNA SNHG14 alleviates LPS-induced inflammation and apoptosis of PC12 cells by regulating miR-181b-5p

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Exp Ther Med. 2021 May;21(5):497. doi: 10.3892/etm.2021.9928. Epub 2021 Mar 17.

ABSTRACT

Spinal cord injury (SCI) is a traumatic central nervous system disorder that leads to permanent functional loss, and unavailable treatment of this disease results in poor quality of life. However, the specific role of long non-coding RNA small nucleolar RNA host gene 14 (lncRNA SNHG14) in SCI has not been fully studied. The aim of the current study was to investigate the role of SNHG14 and its regulatory mechanism in lipopolysaccharide (LPS)-induced PC-12 cells. LPS was used to stimulate PC-12 cells to simulate inflammatory injury following SCI in vitro. Cell viability and apoptosis were respectively assessed by Cell Counting Kit-8 assay and TUNEL assay. Western blotting was performed to detect the expressions of apoptosis-related proteins. The mRNA levels of SNHG14 and microRNA (miR)-181b-5p were detected by reverse transcription-quantitati ve PCR. The target of SNGH14 was predicted by bioinformatics analysis and subsequently validated by a luciferase reporter assay. ELISA was then used to detect the levels of inflammatory factors. The results indicated that LPS induced inflammation, decreased cell viability and increased the apoptosis of PC-12 cells. Interference of SNHG14 alleviated this type of injury of PC-12 cells. Bioinformatics prediction and luciferase reporter assay demonstrated that miR-181b-5p could directly bind to SNHG14. Moreover, mechanistic investigations revealed that the miR-181b-5p inhibitor could reverse the inhibitory effects of SNHG14 silencing on cell viability, inflammation and apoptosis of PC-12 cells. To conclude, the present results showed that SNHG14 knockdown alleviated PC-12 cell inflammation and apoptosis induced by LPS via regulating miR-181b-5p, which might provide a novel insight into the treatment of SCI.

PMID:33791006 | PMC:PMC8005701 | DOI:10.3892/etm.2021.9928

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Cytotoxic, chemosensitizing and radiosensitizing effects of curcumin based on thioredoxin system inhibition in breast cancer cells: 2D vs. 3D cell culture system

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Exp Ther Med. 2021 May;21(5):506. doi: 10.3892/etm.2021.9937. Epub 2021 Mar 18.

ABSTRACT

Targeting the thioredoxin/thioredoxin reductase (Trx/TrxR) system is a promising strategy to overcome cancer resistance to conventional therapy. The present study investigated the effect of curcumin on the Trx/TrxR system either alone or in combination with chemotherapy, or radiotherapy in human MCF-7 breast cancer cells seeded in 2 and 3D culture systems. Cell viability, thioredoxin reductase 1 (TrxR1) activity, and the genetic expression of Trx, TrxR1, Bcl2 and BAX genes were studied. The findings showed that the mode of culture significantly affected the response of cancer cells to different treatment modalities, as well as their gene expression patterns. Curcumin treatment resulted in a reduction of breast cancer cell proliferation and induction of apoptosis, an effect that may be mediated by manipulating Trx system components, mainly Trx expre ssion, and to a lesser extent TrxR1 expression and concentration. Furthermore, curcumin increased the sensitivity of breast cancer cells to chemotherapy and radiotherapy by reducing Trx and TrxR1 expression levels. Thus, curcumin may have a potential role as a dose-modifying agent that can be used either to sensitize resistant cells to therapy or to reduce the dose of these therapeutic agents.

PMID:33791015 | PMC:PMC8005724 | DOI:10.3892/etm.2021.9937

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Application of a three-dimensional (3D) breast cancer model to study macrophage polarization

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Exp Ther Med. 2021 May;21(5):482. doi: 10.3892/etm.2021.9913. Epub 2021 Mar 16.

ABSTRACT

Knowledge of the tumor microenvironment is crucial for developing an effective strategy to treat cancer. Recently, anticancer therapies targeting macrophages have been intensively investigated. Increased understanding of the importance of the tumor microenvironment has led to the development of three-dimensional (3D) in vitro tumor models. However, established techniques for studying tumor-associated macrophages in vitro are limited. We have previously characterized a 3D breast cancer model consisting of breast cancer cells and fibroblasts cocultured on a silk scaffold. In the present study, the influence of this model on macrophage polarization was investigated. The expression of macrophage markers was studied using reverse transcription-quantitative PCR and flow cytometry. The activity of nitric oxide synthase and arginase in macrop hages was also measured. The presented model appeared to induce the polarization of macrophages towards an M2 phenotype. In this 3D tumor model, the in vivo behavior of macrophages could be reproduced. This model may be beneficial for the study of tumor biology and for screening drugs.

PMID:33790991 | PMC:PMC8005691 | DOI:10.3892/etm.2021.9913

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Inhibitory effect of miR-140-5p on doxorubicin resistance of hepatocellular carcinoma

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Exp Ther Med. 2021 May;21(5):507. doi: 10.3892/etm.2021.9938. Epub 2021 Mar 18.

ABSTRACT

To investigate the role of microRNA (miR)-140-5p in doxorubicin (DOX) sensitivity in hepatocellular carcinoma, miR-140-5p and peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1) expression was first evaluated in hepatocellular carcinoma tissues using starBase. Next, in vitro experiments were performed. Cell line expression of miR-140-5p and PIN1 expression was detected by reverse transcription polymerase chain reaction. Cell viability and proliferation were determined by the Cell Counting Kit-8 and EdU assays. The relationship between miR-140-5p and PIN1 was evaluated by TargetScan and a luciferase reporter system. Western blotting was used to detect the expression of PIN1. It was observed that miR-140-5p was downregulated in hepatocellular carcinoma tissues and cell lines compared with normal samples in HCC or normal liver cells. Gain-of-function experiments revealed that miR-140-5p mimics were able to enhance DOX sensitivity of hepatocellular carcinoma cells. Further studies revealed that PIN1 was a target gene of miR-140-5p. Suppression of PIN1 led to higher DOX sensitivity in hepatocellular carcinoma cells. Finally, when comparing a PIN1-siRNA alone group and a PIN1-siRNA plus miR-140-5p inhibitor group, there was no significant difference in cell viability. Furthermore, miR-140-5p mimics did not reduce the sensitivity of PIN1mut plasmid to DOX in HUH7 and SNU449 cells. The present study demonstrated that miR-140-5p could enhance DOX sensitivity in hepatocellular carcinoma cells by targeting PIN1.

PMID:33791016 | PMC:PMC8005744 | DOI:10.3892/etm.2021.9938

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Klotho overexpression suppresses apoptosis by regulating the Hsp70/Akt/Bad pathway in H9c2(2-1) cells

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Exp Ther Med. 2021 May;21(5):486. doi: 10.3892/etm.2021.9917. Epub 2021 Mar 16.

ABSTRACT

Early reperfusion is the most effective and important treatment for acute myocardial infarction. However, reperfusion therapy often leads to a certain degree of myocardial damage. The aim of the present study was to identify the role of klotho, and the molecular mechanism underlying its effects, in myocardial damage using a model of myocardial hypoxia injury. Hypoxia/reoxygenation (H/R) was used to mimic ischemia/reperfusion (I/R) injury in vitro. The expression and distribution of klotho in H9c2(2-1) cells was observed by fluorogenic scanning, and the apoptotic rate was determined by Annexin V-FITC/propidium iodide dual staining. Cell viability was determined by MTT assay, and caspase-3, cleaved caspase-3, Bcl-2, Bax, heat shock protein (Hsp) 70 and Akt levels were assessed by western blotting. A lactate dehydrogenase test was performed to determine the degree of H9c2(2-1) cell damage. The results revealed that klotho was primarily located in the cytoplasm of H9c2(2-1) cells. Klotho overexpression markedly suppressed H/R-induced H9c2(2-1) cell apoptosis. Furthermore, cell viability increased, and injury decreased in response to klotho. Klotho also suppressed the activation of caspase-3, upregulated Bcl2 and decreased Bax levels following H/R injury, as well as alleviating H/R injury by upregulating the expression of Hsp70 and increasing the levels of phosphorylated (p-)Akt and Bad. In conclusion, these results indicate that klotho suppressed H/R-induced H9c2(2-1) cell apoptosis by regulating the levels of Hsp70, p-Akt and p-Bad, which suggest that klotho could be a novel agent for the treatment of coronary disease.

PMID:33790995 | PMC:PMC8005687 | DOI:10.3892/etm.2021.9917

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Bioinformatics analysis of biomarkers of aristolochic acid-induced early nephrotoxicity in embryonic stem cells

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Exp Ther Med. 2021 May;21(5):508. doi: 10.3892/etm.2021.9939. Epub 2021 Mar 18.

ABSTRACT

The present study aimed to identify key genes as potential biomarkers for early nephrotoxicity induced by aristolochic acid (AA) in embryonic stem cells (ESCs). An MTT assay was performed to determine the cytotoxicity of AA in ESCs. Differentially expressed genes (DEGs) were identified using the DNA-Chip Analyzer following microarray analysis. Gene Ontology analysis was performed to determine functional terms enriched by the DEGs in the categories biological process, cellular component and molecular function. Furthermore, the DEGs were subjected to Kyoto Encyclopedia of Genes and Genomes analysis to determine pathways they were accumulated in. Furthermore, a protein-protein interaction network was constructed using Cytoscape 3.2 software. Tumor protein 53 apoptosis effector (Perp), cation transport regulator-like 1 (Chac1), adrenoceptor β2 and Wnt 6 were selected for confirmation by reverse transcription-quantitative (RT-q) PCR analysis. A total of 72 DEGs (49 upregulated and 23 downregulated) were identified. The DEGs were enriched in functional terms and pathways associated with nephrotoxicity and participated in 92 pathways. A total of two hub genes, fructose-1,6-bisphosphatase (Fbp)1 and Fbp2, were filtered out from the interaction network. Perp and phorbol-12-myristate-13-acetate-induced protein 1 were demonstrated to have vital roles in the p53 signaling pathway which was indicated in the interaction network. The results of the RT-qPCR analysis were consistent with the microarray data. Taken together, the present study suggested that hub genes involved in the p53 pathway, including Fbp1, Fbp2 and Perp, may serve as potential biomarkers for early nephrotoxicity induced by AA.

PMID:33791017 | PMC:PMC8005694 | DOI:10.3892/etm.2021.9939

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