Endonasal Odontoidectomy in Basilar Invagination

xlomafota13 shared this article with you from Inoreader Endonasal Odontoidectomy in Basilar Invagination Via leak of cerebrospinal fluid J Neurol Surg B Skull Base. 2021 Feb;82(Suppl 1):S14-S15. doi: 10.1055/s-0040-1714406. Epub 2020 Dec 2. ABSTRACT Objective The endoscopic endonasal odontoidectomy (EEO) is emerging as a feasible surgical alternative to conventional microscopic transoral approach. In this article, we show EEO in the basilar invagination (BI) and describe in detail the technical aspects, advantages, and disadvantages of this approach ( Fig. 1 ). Methods We describe EEO using audiovisual material from the neurosurgical department of Hospital Universitari i Politècnic La Fe Valencia database. Results We present the case of a 61-year-old male patient with BI. Initially, we performed suboccipital decompression and occipitocervical fusion. Subsequently, after a no significant neurological improvement and persistent anterior compression, EEO was performed. The postoperative evolution was uneventful and the preoperative neurological deficits were recovered rapidly after surgery Discussion EEO technique enables complete odontoid resection, preventing invasion of aggressive oral bacterial flora, and it is not limited by the mouth opening. As well, it avoids manipulation of the soft palate, therefore evades the risk of velopalatal insufficiency, facilitates immediate oral tolerance, and early extubation. The rostral position of C1-C2 complex in BI could suppose a great advantage in favor the endonasal approaches. Mucoperichondrial vascularized flaps could be obtained to avoid a postoperative cerebrospinal fluid (CSF) leak and facilitate the reepithelization process of the surgical bed. Conclusion EEO may provide a significant anatomic and technical advantage over the trans-oral approach. The link to the video can be found at: https://youtu.be/Td6MDcjCNKk . PMID:33717804 | PMC:PMC7935722 | DOI:10.1055/s-0040-1714406 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Apoptosis-antagonizing transcription factor is involved in rat post-traumatic epilepsy pathogenesis

xlomafota13 shared this article with you from Inoreader Apoptosis-antagonizing transcription factor is involved in rat post-traumatic epilepsy pathogenesis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):290. doi: 10.3892/etm.2021.9721. Epub 2021 Jan 27. ABSTRACT The present study aimed to explore the pathogenesis behind post-traumatic epilepsy (PTE). In the present study, a chloride ferric injection-induced rat PTE model was established. The expression levels of apoptosis-antagonizing transcription factor (AATF), cleaved caspase-3, p53, Bcl-2 and Bax were measured by western blotting or immunofluorescence staining (IF). The expression of AATF in vivo was downregulated by microinjection of lentiviral-mediated short-hairpin RNA. Compared with control and sham groups, at day 5 after PTE, neuron apoptosis was significantly increased and the expression levels of AATF, p53, cleaved caspase-3 and Bax were significantly upregulated. In addition, IF revealed co-localization of AATF and cleaved caspase-3 in the cortex. Additionally, AATF was expressed mainly in neurons and astrocytes. Following AATF inhibitio n, the expression levels of p53 and cleaved caspase-3 were significantly reduced as compared with the control group. Taken together, these findings suggested that following PTE, AATF is involved in neuronal apoptosis and may serve as a potential target for its alleviation. PMID:33717233 | PMC:PMC7885077 | DOI:10.3892/etm.2021. 9721 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Prenatal diagnosis of a pure 15q distal trisomy derived from a maternal pericentric inversion: A case report

xlomafota13 shared this article with you from Inoreader Prenatal diagnosis of a pure 15q distal trisomy derived from a maternal pericentric inversion: A case report Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):304. doi: 10.3892/etm.2021.9735. Epub 2021 Jan 29. ABSTRACT Distal trisomy or duplication of 15q is a very rare chromosomal disorder; most of the previously reported cases were derived from unbalanced translocations involving chromosome 15 and another chromosome, whereas other mechanisms (e.g. duplication) have rarely been reported. We herein report a very rare prenatal case of a partial 15q trisomy, a 42.64-Mb duplication of 15q22.2-q26.3, arising from a maternal pericentric inversion of chromosome 15 (p11q22) that was not the result of an unbalanced translocation or duplication, and was not associated with concomitant partial monosomy. Fetal ultrasound revealed isolated thickened nuchal translucency at 12 weeks and multiple abnormalities in the second trimester, including early growth restriction, unilateral ventriculomegaly, narrow cavum septi pellucidi with hypoplasia of the corpus callosum, unilateral postaxial polydactyly, clenched hands and clubfoot with clawing of the toes, and a particular general dysplastic and hypotrophic aspect of the heart. The distinctive aspects of the present case may help to refine the phenotype associated with distal duplication 15q. To the best of our knowledge, this is the first report of a prenatal diagnosis with a 15q22.2-q26.3 duplication that did not result from an unbalanced translocation and did not have a concomitant monosomic component. PMID:33717247 | PMC:PMC7885063 | DOI:10.3892/etm.2021.9735 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Analysis of the cytotoxic effects, cellular uptake and cellular distribution of paclitaxel-loaded nanoparticles in glioblastoma cells in vitro

xlomafota13 shared this article with you from Inoreader Analysis of the cytotoxic effects, cellular uptake and cellular distribution of paclitaxel-loaded nanoparticles in glioblastoma cells <em>in vitro</em> Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):292. doi: 10.3892/etm.2021.9723. Epub 2021 Jan 27. ABSTRACT Glioblastoma is the most common and aggressive type of brain tumor. Although treatments for glioblastoma have been improved recently, patients still suffer from local recurrence in addition to poor prognosis. Previous studies have indicated that the efficacy of chemotherapeutic or bioactive agents is severely compromised by the blood-brain barrier and the inherent drug resistance of glioblastoma. The present study developed a delivery system to improve the efficiency of delivering therapeutic agents into glioblastoma cells. The anticancer drug paclitaxel (PTX) was packed into nanoparticles that were composed of amphiphilic poly (γ-glutamic-acid-maleimide-co-L-lactide)-1,2-dipalmitoylsn-glycero-3-phosphoethanolaminecopolymer conjugated with targeting moiety transferrin (Tf). The Tf nanoparticles (Tf-NPs) may enter glioblastoma cells via transferrin receptor-mediated endocytosis. MTT assay and flow cytometry were used to explore the cytotoxic effects, cellular uptake and cellular distribution of paclitaxel-loaded nanoparticles. The results indicated that both PTX and PTX-Tf-NPs inhibited the viability of rat glioblastoma C6 cells in a dose-dependent manner, but the PTX-Tf-NPs exhibited a greater inhibitory effect compared with PTX, even at higher concentrations (0.4, 2 and 10 µg/ml). However, both PTX and PTX-Tf-NPs exhibited a reduced inhibitory effect on the viability of mouse hippocampal neuronal HT22 cells compared with that on C6 cells. Additionally, in contrast to PTX alone, PTX-Tf-NPs treatment of C6 cells at lower concentrations (0.0032, 0.0160 and 0.0800 µg/ml) induced increased G2/M arrest, although this difference did not occur at a higher drug concentration (0.4 µg/ml). It was observed that FITC-labeled PTX-Tf-NPs were endocytosed by C6 cells within 4 h. Furthermore, FITC-labeled PTX-Tf-NPs or Tf-NPs co-localized with a lysosomal tracker, Lysotracker Red DND-99. These results of the present study indicated that Tf-NPs enhanced the cytotoxicity of PTX in glioblastoma C6 cells, suggesting that PTX-Tf-NPs should be further explored in animal models of glioblastoma. PMID:33717235 | PMC:PMC7885080 | DOI:10.3892/etm.2021.9723 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Low KRT15 expression is associated with poor prognosis in patients with breast invasive carcinoma

xlomafota13 shared this article with you from Inoreader Low KRT15 expression is associated with poor prognosis in patients with breast invasive carcinoma Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):305. doi: 10.3892/etm.2021.9736. Epub 2021 Jan 29. ABSTRACT Although keratin 15 (KRT15) has been indicated to be overexpressed in several types of tumor, its role in breast invasive carcinoma (BRCA) has so far remained elusive. The aim of the present study was to explore KRT15 expression in BRCA based on data obtained from The Cancer Genome Atlas and The Genotype-Tissue Expression. KRT15 expression was compared using a Wilcoxon rank-sum test. Functional enrichment analysis was performed to reveal the biological roles and pathways of KRT15. The association between KRT15 expression and immune-cell infiltration was evaluated via single-sample gene set enrichment analysis (ssGSEA). To investigate the relationship between clinicopathological features and KRT15 expression, the prognostic value of KRT15 and other clinical factors was evaluated using Cox regression analysis and Kaplan-Meier (KM) plots. Subgroup pro gnostic analysis was also performed using forest plots and KM curves. Finally, a tissue microarray was used to assess KRT15 expression in BRCA tissues. KRT15 expression was significantly lower in BRCA tissues compared with that in normal tissues. Functional enrichment analysis suggested that KRT15-related genes were primarily enriched in the transmembrane transporter complex, cornification and ligand-receptor interactions. Increased KRT15 was associated with several tumor-suppressive pathways. ssGSEA revealed that high KRT15 expression was significantly associated with natural killer-cell, B-cell and mast-cell infiltration. Significant associations were observed between low KRT15 expression and advanced stage clinicopathological factors, as well as unfavorable overall survival (OS) and disease-specific survival. Multivariate Cox regression analysis suggested that KRT15 was an independent prognostic factor for OS (P=0.039; hazard ratio, 0.590; 95% CI, 0.358-0.974). Subgroup prognosti c analysis demonstrated that low KRT15 was a reliable predictor of poor OS. Immunohistochemistry of a tissue microarray indicated that positive KRT15 expression rates were significantly higher in normal tissues compared with those in the BRCA tissues. In conclusion, low KRT15 expression was significantly associated with poor prognosis in patients with BRCA. Thus, KRT15 may serve an important role in BRCA progression and may be used as a promising prognostic marker for diagnostic and prognostic analyses in patients with BRCA. PMID:33717248 | PMC:PMC7885068 | DOI:10.3892/etm.2021.9736 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Biological effects of NODAL on endometrial cancer cells and its underlying mechanisms

xlomafota13 shared this article with you from Inoreader Biological effects of NODAL on endometrial cancer cells and its underlying mechanisms Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):402. doi: 10.3892/etm.2021.9833. Epub 2021 Feb 25. ABSTRACT Activin A receptor type 1C (ALK7) and its ligand nodal growth differentiation factor (NODAL) serve numerous roles in cancer cells, including regulating cancer invasion, migration and apoptosis. NODAL promotes breast cancer cell apoptosis by activating ALK7; however, ALK7 and NODAL expression in endometrial cancer (EC), as well as their effects and underlying mechanisms in EC cells, are not completely understood. The present study aimed to characterize the expression of NODAL and ALK7 in EC, as well as the underlying mechanisms. The expression levels of ALK7 and NODAL were detected via reverse transcription-quantitative PCR and western blotting. Cell transfection was performed to overexpress NODAL or interfere ALK7. Cell proliferation, invasion and migration were detected via Cell Counting Kit-8, Transwell and wound healing assays, respectively. Flo w cytometry was performed to detect cell apoptosis and western blotting was conducted to detect the expression levels of apoptosis-related proteins. NODAL and ALK7 expression levels were significantly decreased in EC cell lines compared with normal endometrial cells. NODAL overexpression inhibited EC cell proliferation, invasion and migration, and promoted EC cell apoptosis compared with the overexpression-negative control (Ov-NC) group. Moreover, NODAL overexpression significantly increased ALK7 expression levels in EC cells compared with the Ov-NC group. ALK7 reversed NODAL overexpression-mediated inhibition of EC cell proliferation, invasion and migration, and promotion of EC cell apoptosis. The present study indicated that NODAL inhibited EC cell proliferation, invasion and migration, and promoted EC cell apoptosis by activating ALK7. PMID:33717261 | PMC:PMC7938447 | DOI:10.3892/etm.2021.9833 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

The complex relationship between infertility and psychological distress (Review)

xlomafota13 shared this article with you from Inoreader The complex relationship between infertility and psychological distress (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):306. doi: 10.3892/etm.2021.9737. Epub 2021 Feb 1. ABSTRACT Infertility is defined as the inability to procreate, or carry or deliver a baby naturally. The majority of specialists describe infertility as being unable to get pregnant after having tried for at least one year. The relationship between infertility and psychological stress is complex. On the one hand, infertile couples are subject to greater stress and have a greater risk of developing psychological disorders compared with normal, healthy couples. On the other hand, high levels of psychological distress have been indicated to increase infertility. Therefore, in the present review, the main factors that may lead to increased stress in couples who try to conceive, psychological stress as the reason for infertility, and the therapies that can help decrease psychological distress and increase chances of pregnancy are underlined. In addition to the ps ychological side effects that may occur from infertility itself, a range of other side effects can be caused by hormones and drugs used to treat infertility. Additionally, problem during erection and ejaculation can cause of psychological distress, which can lead to infertility among men. Psychotherapy is the main intervention recommended for couples who suffer from any form of infertility. Ideally, counselling should begin before patients start any medical intervention to help with their infertility. PMID:33717249 | PMC:PMC7885086 | DOI:10.3892/etm.2021.9737 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

miR-146b correlates with increased disease activity and psoriatic tissue inflammation and promotes keratinocyte proliferation in psoriasis

xlomafota13 shared this article with you from Inoreader miR-146b correlates with increased disease activity and psoriatic tissue inflammation and promotes keratinocyte proliferation in psoriasis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):296. doi: 10.3892/etm.2021.9727. Epub 2021 Jan 28. ABSTRACT The present study aimed to investigate the expression of microRNA (miR)-146b in psoriatic tissue and its correlation with psoriasis activity and inflammation. The effect of miR-146b overexpression on keratinocyte proliferation and apoptosis was also explored. The expression of miR-146b in the psoriasis-affected tissue and non-affected tissue of 110 patients was determined via reverse transcription-quantitative (RT-q)PCR. The psoriasis-affected body surface area and psoriasis area severity index (PASI) score were recorded for evaluating disease activity. The expression of various inflammatory cytokines in psoriasis-affected tissue was also detected via RT-qPCR. miR-146b overexpression and control plasmids were constructed and transfected into HaCaT cells in vitro. Subsequently, cell proliferation, apoptosis and tumor necrosis factor (TNF)-rel ated apoptosis-inducing ligand (TRAIL)-induced cell apoptosis were determined. The results revealed that the expression of miR-146b was increased in psoriasis-affected tissue compared with that in unaffected tissue. The results obtained from a receiver operating characteristic curve analysis demonstrated that miR-146b levels were able to discriminate between psoriasis-affected tissue and unaffected tissue, with an area under the curve value of 0.781 (95% CI: 0.720-0.843). In addition, miR-146b expression in psoriatic tissue was correlated with an increased PASI score in patients with psoriasis. miR-146b expression in psoriatic tissue was positively correlated with TNF-α, interleukin (IL)-6 and IL-17 mRNA levels. In vitro, miR-146b overexpression enhanced HaCaT cell proliferation and suppressed apoptosis as well as TRAIL-induced apoptosis when compared with that in control-transfected HaCaT cells. In conclusion, miR-146b was positively correlated with disease activity and pso riatic tissue inflammation. Keratinocyte proliferation was also promoted in psoriasis. PMID:33717239 | PMC:PMC7885075 | DOI:10.3892/etm.2021.9727 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Long non-coding RNA FOXD2-AS1 promotes proliferation, migration and invasion of ovarian cancer cells via regulating the expression of miR-4492

xlomafota13 shared this article with you from Inoreader Long non-coding RNA FOXD2-AS1 promotes proliferation, migration and invasion of ovarian cancer cells via regulating the expression of miR-4492 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):307. doi: 10.3892/etm.2021.9738. Epub 2021 Feb 1. ABSTRACT The aim of the present study was to determine the role of long non-coding RNA (lncRNA) forkhead box D2 antisense 1 (FOXD2-AS1) in the development of ovarian cancer, investigate the underlying mechanisms and provide a potential diagnostic biomarker for ovarian cancer. A total of 39 ovarian cancer patients were included, and the ovarian cancer tissues and paracancer tissues were obtained. The ovarian cancer cell lines SKOV3 and OVCAR3 and the human ovarian normal epithelial cell line IOSE80 were cultured. The expression of lncRNA FOXD2-AS1 and miR-4492 was detected by reverse transcription-quantitative PCR. Small interfering RNA targeting FOXD2-AS1 (si-FOXD2-AS1), microRNA (miR)-4492 mimics, miR-4492 inhibitor and their corresponding controls were transfected into cells. The proliferation was detected with a Cell-Couting-Kit-8 assay, and migration and invasion were determined using Transwell assays. The mutual binding site of lncRNA FOXD2-AS1 and miR-4492 was predicted with the miRDB database and verified by a luciferase reporter assay. Finally, a rescue assay was performed. The results suggested that lncRNA FOXD2-AS1 was upregulated in ovarian cancer tissues and cell lines. si-FOXD2-AS1 was able to inhibit the proliferation, migration and invasion of ovarian cancer cells. lncRNA FOXD2-AS1 was confirmed to directly target miR-4492. The expression of lncRNA FOXD2-AS1 and miR-4492 exhibited a negative correlation. In a rescue experiment, miR-4492 inhibitor abrogated the effect of siFOXD2-AS1 in SKOV3 and OVCAR3 cell lines. In conclusion, lncRNA FOXD2-AS1 promotes the proliferation and invasion of ovarian cancer cells via regulating the expression of miR-4492. It may be a novel potential diagnostic biomarker and therapeutic target for ovarian cancer. PMID:33717250 | PMC:PMC7885078 | DOI:10.3892/etm.2021.9738 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Integrated bioinformatics analysis for the identification of key genes and signaling pathways in thyroid carcinoma

xlomafota13 shared this article with you from Inoreader Integrated bioinformatics analysis for the identification of key genes and signaling pathways in thyroid carcinoma Via Experimental and therapeutic medicine Exp Ther Med. 2021 Apr;21(4):298. doi: 10.3892/etm.2021.9729. Epub 2021 Jan 28. ABSTRACT Thyroid carcinoma (TC) is one of the most common types of endocrine neoplasm with poor prognosis due to its aggressive behavior. Biomarkers for early diagnosis and prevention of TC are in urgent demand. By using a bioinformatics analysis, the present study aimed to identify essential genes and pathways associated with TC. First, the GSE27155 and GSE50901 expression profiles were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were obtained using the two microarray datasets and further subjected to integrated analysis. A gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed 45 common DEGs in the two datasets. GO and KEGG pathway analysis indicated that the biological functions of the DEGs included protein binding, cardiac muscle cell potential involved i n contraction, aldehyde dehydrogenase activity, the TGF-β receptor signaling pathway and the canonical Wnt signaling pathway. A protein-protein interaction network was also constructed and visualized to display the nodes of the top 9 up- and 36 downregulated common DEGs. The integrated bioinformatics analysis indicated that potassium inwardly rectifying channel subfamily J member 2 (KCNJ2) was the most significantly upregulated DEG. The transcriptional levels of KCNJ2 were confirmed to be elevated in TC tissues compared with those in normal tissues using reverse transcription-quantitative PCR analysis. Furthermore, the expression level of KCNJ2 was significantly associated with the 5-year survival rate of patients with TC, which was determined using the Kaplan-Meier method. In TC cell lines, KCNJ2 was also upregulated as compared with that in a normal control cell line. Finally, small interfering RNA was used to knock down the expression of KCNJ2, which was demonstrated to inhibit cell proliferation, migration and invasion, while increasing apoptosis in TC cells. In conclusion, in the present study, KCNJ2 was screened as an oncogene with a crucial role in TC development and progression and may represent a promising candidate biomarker and therapeutic target for TC. PMID:33717241 | PMC:PMC7885060 | DOI:1 0.3892/etm.2021.9729 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.