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Δευτέρα 1 Νοεμβρίου 2021

3D-4K exoscope-assisted temporal bone dissection: a new frontier in surgical training

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Eur Arch Otorhinolaryngol. 2021 Oct 31. doi: 10.1007/s00405-021-07137-1. Online ahead of print.

ABSTRACT

PURPOSE: To assess if 3D-4K exoscope is a valuable tool for temporal bone dissection and to evaluate its teaching potential.

METHODS: Six consecutive 3D-4K-exoscope-assisted cortical mastoidectomies were performed by a novice, an intermediate and an expert surgeon (two dissections each). All dissections were entirely recorded and later evaluated independently by three other experienced surgeons. The dissection end-product was evaluated according to the Melbourne Mastoidectomy Scale (MMS). Paired t test was used to assess whether novice and intermediate surgeons have a score improvement in the second dissection compared to the first one. Surgeons' interactions, depth effect, and 3D impression were also assessed to perform a subjective analysis.

RESULTS: Mean MMS scores for the novice, intermediate and expert surgeon were 11.3 ± 2.8, 13.8 ± 3.9 and 19 ± 1.3, respectively. Paired t test demonstrated a statically significant improvement between the first and the second dissection both for the novice and the intermediate surgeon (+ 4.7 and + 7 points; p = 0.0002). A high-quality magnification of the temporal bone was obtained, allowing the expert surgeon to identify all the anatomical structures without injuring them. The exoscope was capable of providing a high involvement in the dissections with very effective interactions between the expert surgeon and the trainees, that had access to the same surgical field view.

CONCLUSION: 3D-4K-exoscope resulted adequate for a safe and effective mastoidectomy and showed a high potential for training and educational purposes. It can represent a valid option for surgical training of temporal bone dissection and a new interactive tool to understand the complex temporal bone anatomy.

PMID:34719728 | DOI:10.1007/s00405-021-07137-1

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MicroRNA-424 alleviates neurocyte injury by targeting PDCD4 in a cellular model of cerebral ischemic stroke

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Exp Ther Med. 2021 Dec;22(6):1453. doi: 10.3892/etm.2021.10888. Epub 2021 Oct 15.

ABSTRACT

Cerebral ischemic stroke is the primary cause of stroke-associated mortality and disability, and current therapeutic options are limited and ineffective. The present study aimed to investigate the potential of apoptotic therapy and the role of microRNA (miR)-424 in cerebral ischemic stroke. PC12 cells, a cloned cell line from rat adrenal pheochromocytoma, were treated with CoCl2 to construct a cellular ischemia model. mRNA and protein levels of programmed cell death protein 4 (PDCD4), Bcl-2, Bax, caspase-3, PI3K and AKT were evaluated using reverse transcription-quantitative PCR and western blot analyses, respectively. Cell Counting Kit-8 assays were performed to examine cell viability in the ischemia model. Flow cytometry was conducted to evaluate the apoptosis of ischemic cells. Furthermore, a luciferase assay was performed to verify the target gene of miR-424. It was revealed that the expression level of miR-424 was downregulated in the ischemia model, while the expression of PDCD4 was upregulated. Moreover, the expression of miR-424 was increased after treatment with miR-424 mimics. The mRNA and protein expression of PDCD4 was upregulated after transfection with pcDNA3.1-PDCD4. PDCD4 was predicted and demonstrated to be a target of miR-424. Notably, overexpression of miR-424 increased cell viability and inhibited apoptosis in the ischemia model, which was reversed by co-treatment with pcDNA3.1-PDCD4. Furthermore, overexpression of miR-424 regulated the expression of PDCD4, Bax, Bcl-2, phosphorylated-PI3K/AKT and caspase-3, which was restored after co-transfection with pcDNA3.1-PDCD4. Collectively, the results indicated that miR-424 regulated the progression of cerebral ischemic stroke in a cellular model by targeting PDCD4.

PMID:34721695 | PMC:PMC8549098 | DOI:10.3892/etm.2021.10888

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Pueratin improves diminished ovarian reserve by inhibiting apoptosis

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Exp Ther Med. 2021 Dec;22(6):1423. doi: 10.3892/etm.2021.10858. Epub 2021 Oct 11.

ABSTRACT

Pueratin (Pue) is an extract from Pueraria lobata, and exhibits therapeutic effects for the treatment of inflammation. However, the beneficial effects and mechanisms underlying Pue in the treatment of diminished ovarian reserve (DOR) remains to be fully elucidated. The aim of the present study was to investigate the effect of Pue on Bcl-2 and Bax protein expression in rats with DOR, associated with infertility within clinical practice, induced by 4-vinylcyclohexene diepoxide (VCD). A model of DOR was established in female Sprague Dawley rats by an intraperitoneal injection of 80 mg/kg VCD daily for 45 days. From day 1, the Sprague Dawley rats were orally administered with drugs daily for 45 days. They were divided into normal, model, Pue-low dose (L), Pue-medium dose (M) and Pue-high dose (H) groups (50, 100 and 300 mg/kg Pue, respectively). Foll icle-stimulating hormone (FSH), luteinizing hormone (LH) and estradiol (E2) levels were subsequently detected using ELISA. H&E staining and TUNEL staining were used to evaluate histopathological changes and apoptosis levels in the ovary, respectively. Bcl-2 and Bax protein expression levels in rat ovaries were evaluated using immunohistochemistry and western blotting. Compared with those in the model group, FSH and LH levels in the Pue-L, -M and -H groups were significantly decreased, whilst E2 levels were significantly increased (P<0.05). After intragastric administration, the volume of the ovaries and uteri of rats in the Pue groups was increased compared with the model group, and the numbers of primordial follicles and primary follicles were also increased. The number of apoptotic cells and the expression of Bax were significantly reduced in a dose-dependent manner (P<0.05), compared with the model group. In addition, Bcl-2 protein expression and t he Bcl-2/Bax ratio were found to be significantly increased in the Pue-treated groups in a dose-dependent manner (P<0.05), compared with the model group. In conclusion, Pue treatment improved ovarian function by regulating hormone balance in addition to Bcl-2 and Bax expression.

PMID:34721677 | PMC:PMC8549093 | DOI:10.3892/etm.2021.10858

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MicroRNA-98-5p inhibits human mesangial cell proliferation and TNF-α and IL-6 secretion by targeting BTB and CNC homology 1

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Exp Ther Med. 2021 Dec;22(6):1436. doi: 10.3892/etm.2021.10871. Epub 2021 Oct 12.

ABSTRACT

MicroRNA (miR)-98-5p has been reported to be involved in the development of lupus nephritis (LN); however, its specific role in LN remains unclear. The present study aimed to investigate the effect of miR-98-5p on human mesangial cell proliferation and the secretion of TNF-α and IL-6. Reverse transcription-quantitative PCR (RT-qPCR) and western blotting were used to analyze the level of gene and protein expression, respectively. Cellular proliferation was assessed using a Cell Counting Kit-8 (CCK-8) assay. ELISA was used to detect the secretion of TNF-α and IL-6 by human mesangial cells. RT-qPCR analysis revealed that miR-98-5p expression was downregulated in LN renal tissues compared with control renal tissues. Overexpression of miR-98-5p inhibited human mesangial cell proliferation and the secretion of TNF-α and IL-6, whereas miR-98-5p-knock down demonstrated the opposite effect. Dual luciferase reporter assays demonstrated that miR-98-5p directly targeted BTB and CNC homology 1 (BACH1). BACH1-overexpression promoted human mesangial cell proliferation and the secretion of TNF-α and IL-6, whereas BACH1-knockdown demonstrated the opposite effect. Notably, co-transfection with miR-98-5p mimic inhibited BACH1-overexpression induced human mesangial cell proliferation and the secretion of TNF-α and IL-6. The results of the present study indicated that miR-98-5p inhibited human mesangial cell proliferation and the secretion of TNF-α and IL-6 by targeting BACH1. Therefore, miR-98-5p and BACH1 may represent potential therapeutic targets for LN.

PMID:34721678 | PMC:PMC8549099 | DOI:10.3892/etm.2021.10871

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Low-activity 125I implantation into VX2 tumor rabbits and quantitative evaluation of the precise therapeutic effect

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Exp Ther Med. 2021 Dec;22(6):1438. doi: 10.3892/etm.2021.10873. Epub 2021 Oct 12.

ABSTRACT

There is still controversy about quantitatively evaluating the therapeutic effect of radioactive low-activity iodine-125 seeds (125I seeds). In the present study, a paired VX2 tumor model in a rabbit hind leg muscle was established, which is virus-induced anaplastic squamous cell carcinoma characterized by hypervascularity, rapid growth and easy propagation in the skeletal muscle. 125I seeds with 0.4 and 0.7 mCi activity were implanted into the left and right legs, respectively, using a radiation treatment planning system under positron emission tomography (PET)/computed tomography (CT) guidance. PET/CT scans and hematoxylin and eosin staining were observed at 72 h and 2 and 4 weeks after implantation to assess the therapeutic effect. The results showed that the average tumor length and standard uptake valu e (SUV) decreased over time, and both 125I seed groups achieved therapeutic effects at 4 weeks post-implantation. Quantitative evaluation of tumor inhibition rate, SUV variation and tumor marker ratio (Bcl-2/Bax) suggested that 0.7 mCi 125I seeds were more suitable than 0.4 mCi seeds in a clinical setting.

PMID:34721680 | PMC:PMC8549107 | DOI:10 .3892/etm.2021.10873

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Huoxue Qianyang Qutan recipe attenuates Ang II-induced cardiomyocyte hypertrophy by regulating reactive oxygen species production

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Exp Ther Med. 2021 Dec;22(6):1446. doi: 10.3892/etm.2021.10881. Epub 2021 Oct 14.

ABSTRACT

Continuous and irreversible cardiac hypertrophy can induce cardiac maladaptation and cardiac remodeling, resulting in increased risk of developing cardiovascular diseases. The present study was conducted to investigate the therapeutic effect of Huoxue Qianyang Qutan recipe (HQQR) on angiotensin II (Ang II)-induced cardiomyocyte hypertrophy. Primary cardiomyocytes were isolated from the cardiac tissue of neonatal rats, followed by flow cytometry detection to confirm the proportion of primary cardiomyocytes. Cell Counting Kit-8 assay and immunofluorescence detection were performed to examine the effect of Ang II and HQQR on cardiomyocyte hypertrophy. Reactive oxygen species (ROS) and a series of metabolic indicators were quantified to investigate the effect of HQQR on Ang II-induced cardiomyocyte hypertrophy. Mitochondrial electron transport chain complex activity and related coding gene expression were determined to explore the effect of HQQR on mitochondrial function. HQQR significantly inhibited Ang II-induced cardiomyocyte hypertrophy and restored Ang II-induced ROS accumulation, metabolic indicators, and membrane potential levels. HQQR also regulated the mitochondrial function related to the sirtuin 1 pathway in Ang II-induced cardiomyocytes by increasing the activity of the mitochondrial electron transport chain complex and affecting the expression of genes encoding mitochondrial electron transport chain complex subunits. HQQR could alleviate Ang II-induced cardiomyocyte hypertrophy by modulating oxidative stress, accumulating ROS and increasing mitochondrial electron transport chain activity.

PMID:34721688 | PMC:PMC8549094 | DOI:10.3892/etm.2021.10881

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Low-doses of aspirin promote the growth of human PC-9 lung cancer cells through activation of the MAPK family

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Exp Ther Med. 2021 Dec;22(6):1440. doi: 10.3892/etm.2021.10875. Epub 2021 Oct 12.

ABSTRACT

Aspirin has been reported for its anti-tumor activity, however, there are few studies on its effects in lung cancer. The present study found that aspirin had a dual role in the proliferation of human lung cancer PC-9 (formerly known as PC-14) and A549 cells, and in human colon cancer HCT116 cells. The cells were treated with 0, 1, 2, 4, 8 and 16 mM aspirin for 24-72 h or 7-12 days and cell proliferation was examined by MTT and colony formation assay. In order to explore the relationship between the proliferation-enhancing effect of low-dose aspirin and mitogen-activated protein kinase (MAPK) signaling activation, PC-9 cells were pretreated with 10 µM PD98059 (a specific inhibitor of ERK), SB203580 (a specific inhibitor of p38) and SP600125 (a specific inhibitor of JNK) for 30 min respectively. Western blot assay was performed to detect the activ ation of MAPK members in PC-9 cells. Cellular apoptosis was detected using flow cytometer-based Annexin V/propidium iodide dual staining. An assessment of MAPK inhibitors was performed to further validate the role of JNK, p38 and ERK in aspirin-promoted PC-9 cell growth. It was demonstrated that aspirin could promote the growth of human PC-9 lung cancer cells and induced MAPK activation at low concentrations. All the MAPK inhibitors tested (PD98059, SB203580 and SP600125) were able to inhibit the aspirin-induced proliferation of PC-9 cells.

PMID:34721682 | PMC:PMC8549104 | DOI:10.3892/etm.2021.10875

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Identification and functional annotation of differentially expressed long noncoding RNAs in retinoblastoma

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Exp Ther Med. 2021 Dec;22(6):1447. doi: 10.3892/etm.2021.10882. Epub 2021 Oct 14.

ABSTRACT

Retinoblastoma (RB), the most common intraocular malignancy, typically occurs in pediatric patients under the age of 6 years. The present study aimed to explore the long noncoding RNA (lncRNA) expression profile in RB and identify novel lncRNA biomarkers to facilitate the investigation of molecular mechanisms of RB and improve clinical therapy. Raw microarray data for the comparison of gene expression between three RB and three adjacent normal tissue samples were downloaded from Gene Expression Omnibus (dataset no. GSE111168). After identification of differentially expressed lncRNAs (DELs) and differentially expressed mRNAs (DEMs) in RB, functional enrichment analyses and a DEL-DEM weighted correlation network analysis were performed. A total of 3,915 DELs (1,774 upregulated and 2,141 downregulated) and 3,715 DEMs (1,492 upregulated and 2,223 dow nregulated) were identified in RB. The DEL-targeted DEMs were highly enriched by genes involved in hexose transport, muscle tissue morphogenesis, the stereocilium membrane, endothelin B receptor binding and γ-filamin/ABP-L, α-actinin and telethonin binding protein of the Z-disc binding. Furthermore, associations of the DELs and DEMs with several pathways were determined, including PI3K/AKT, Hippo and cancer signaling, as well as extracellular matrix-receptor interaction pathways. Coexpression network analysis revealed that the top three DELs, lnc-DAZ1-161, lnc-HDAC7-21 and lnc-OR52A1-55, formed coexpression modules with 181, 156 and 210 DEMs, respectively. In addition, the top three DEMs, namely EIF1AY, GSTM1 and NLRP11, formed coexpression modules with 33, 50 and 41 DELs, respectively. Validation using reverse transcription-quantitative PCR indicated that the expression of representative lncRNAs (lnc-DAZ1-161 and lnc-HDAC7-21) in RB cells in vitro was consistent with that in RB tissues in the database, while the expression of lnc-OR52A1-55 was not consistent with the database. These results suggested that the aberrant lncRNA expression profile in RB is related to the differential regulation of numerous physiological and pathological processes. The lncRNA and mRNA profiles in RB identified may provide novel targets for the investigation of its molecular mechanisms and thus lead to improvements in clinical therapy for RB.

PMID:34721689 | PMC:PMC 8549103 | DOI:10.3892/etm.2021.10882

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Repeated exposure to sevoflurane in neonatal rats impairs cognition in adulthood via the PKA-CREB-BDNF signaling pathway

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Exp Ther Med. 2021 Dec;22(6):1442. doi: 10.3892/etm.2021.10877. Epub 2021 Oct 13.

ABSTRACT

Sevoflurane (Sev) anesthesia is widely used in pediatrics due to its low blood-gas partition coefficient and lack of pungency. However, Sev treatment may lead to cognitive dysfunction in later life. The current study administered Sev to neonatal rats to investigate the effects of Sev treatment on cognitive performance in adulthood. In total, 6-day-old rats received 3% Sev for 2 h daily for 3 consecutive days. The cognitive function of rats in adulthood was evaluated in 56-day-old rats by Morris water maze test. The hippocampal neuron morphology was observed by Nissl staining. Hippocampal brain-derived neurotrophic factor (BDNF) levels were measured by ELISA. The protein expression of protein kinase A (PKA), cAMP response element binding protein (CREB), phosphorylated-CREB (p-CREB) and BDNF in hippocampus were assessed by western blotting. The wat er maze results demonstrated that neonatal treatment with Sev resulted in a significant impairment of cognition in 56-day-old adult rats. Behavioral analysis revealed that Sev treatment increased latency to first pass the platform and decreased residence in target quadrants and across platform frequency compared with the control group in Morris water maze tests. Furthermore, compared with the control group, neonatal exposure to Sev reduced the number of neurons and the concentration of BDNF in the hippocampus, a brain region important for learning and memory. Additionally, Sev significantly decreased the expression of PKA, p-CREB, BDNF and the p-CREB/CREB ratio. Treatment with bucladesine, a selective PKA agonist, partially reversed the deleterious effects of Sev. In summary, the results indicated that PKA-CREB-BDNF signaling served an important role in the cognitive decline caused by neonatal exposure to Sev.

PMID:34721684 | PMC:PMC8549089 | DOI:10.3892/etm.2021.10877

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miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2

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Exp Ther Med. 2021 Dec;22(6):1448. doi: 10.3892/etm.2021.10883. Epub 2021 Oct 14.

ABSTRACT

[This retracts the article DOI: 10.3892/etm.2017.4608.].

PMID:34721690 | PMC:PMC8549096 | DOI:10.3892/etm.2021.10883

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Overactive bladder: A review and update

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Exp Ther Med. 2021 Dec;22(6):1444. doi: 10.3892/etm.2021.10879. Epub 2021 Oct 14.

ABSTRACT

Overactive bladder syndrome is a chronic, disabling condition with physical, psychological and social consequences that significantly affects the quality of life of millions of patients worldwide. The economic impact of this disorder is crucial. Overactive bladder syndrome is a little-known condition, with different manifestations from patient to patient, which causes a great deal of frustration to the medical staff involved. The patient requires a clear explanation and the full support of the attending physician. It is extremely important to establish a correct diagnosis and an effective individualized treatment. The collaboration and understanding of these patients are extremely important aspects. Improving the quality of life in these patients is the main purpose in managing this condition. There are several treatment modalities that may be us ed progressively, with favorable albeit inconsistent results. This condition remains extremely challenging for specialists and, unfortunately, always one of maximum interest.

PMID:34721686 | PMC:PMC8549091 | DOI:10.3892/etm.2021.10879

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