Sensor-based cloud computing data system and long distance running fatigue assessment.

Wireless sensor networks are widely used in sports training, medical and health care, smart home, environmental monitoring, cloud data and other fields because of their large scale, self-organization, reliability, dynamic, integration and data centralization. Based on this point, this article conducts a comprehensive analysis and research on cloud computing data systems, and designs and implements a dynamic replication strategy. Since different users have different demands for different data at different times, it is necessary to record and analyze recent users' data access, so as to actively adjust the number and location of data blocks. Subsequently, a multi-source blockchain transmission method was proposed and implemented, which can significantly reduce the time cost of data migration and improve the overall performance of cloud storage data systems. Finally, the article provides an in-depth analysis of long-distance running fatigue. This study will design a simulated specialized exercise load experiment to reproduce the load characteristics of excellent athletes during mid to long distance running, in order to induce exercise fatigue in the main muscles of different parts of their bodies. At the same time, the amplitude frequency joint analysis of the surface changes of EMG signal in this process is carried out. This article conducts research on sensor based cloud computing data systems and long-distance running fatigue assessment, promoting the development of cloud computing data systems and improving long-distance running fatigue assessment methods.

Comparison between postauricular steroid injection and intratympanic steroid perfusion for refractory severe and profound sudden sensorineural hearing loss.

BACKGROUND: To analyze the clinical efficacy of intratympanic steroid perfusion (ISP) and postauricular steroid injection (PSI) for refractory severe and profound sudden sensorineural hearing loss (SSNHL). METHODS: SSNHL patients who failed a conventional treatment with severe to profound hearing loss [pure tone average (PTA, 0.25-8 kHz) > 60 dB] were treated with ISP or PSI plus antioxidant and neurotrophin for 10 consecutive days. Antioxidant and neurotrophin were administrated either intravenously and/or orally. All patients were assigned into the ISP group or the PSI group and followed up for more than three months. The changes in PTA, effective rate and side effects were analyzed in the two groups. RESULTS: Similar hearing improvements and effective rates were observed in the two groups. However, a slightly better efficacy was observed in the PSI group compared to the ISP group. Patients with shorter intervals from onset to treatment had significantly more hearing improvements. The route of antioxidant and neurotrophin administration had no impact on treatment effects. CONCLUSION: Both ISP and PSI could be used as salvage treatments for refractory SSNHL. These salvage treatments should be started as soon as possible once SSNHL patients fail a conventional treatment.

Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress.

BACKGROUND: To analyze mechanisms of action of glucocorticoid treatment for endoplasmic reticulum stress (ERS) in sensorineural hearing loss (SNHL), we aimed to evaluate the expression and activation status of the protein kinase RNA-like ER kinase (PERK)-C/EBP homologous protein (CHOP) pathway, which is the major pathway in the ERS. METHODS: In the present study, we established an in vitro ERS model using tunicamycin-treated hair-cell-like HEI-OC1 cells. The effect of dexamethasone on proliferation inhibition, apoptosis, and ATF4-CHOP pathway in HEI-OC1 cells was examined by CCK-8 assay, flow cytometry, western blotting, and reverse transcription PCR, respectively. RESULTS: In HEI-OC1 cells, dexamethasone was shown to significantly reduce the tunicamycin-induced expression of ATF4 and CHOP in the context of sustained viability and proliferation, a therapeutic effect that was reversible by co-treatment with a glucocorticoid antagonist. CONCLUSION: Dexamethasone can protect hair-cell-like HEI-OC1 cells from ERS damage, which may be one of the mechanisms of action for GCs in SNHL treatment.

Elucidation of the Hdac2/Sp1/miR-204-5p/Bcl-2 axis as a modulator of cochlear apoptosis via in vivo/in vitro models of acute hearing loss.

We previously reported that dysregulation of histone deacetylase 2 (Hdac2) was associated with the prognosis of sudden sensorineural hearing loss. However, the underlying molecular mechanisms are poorly understood. In the present study, we developed an acute hearing loss animal model in guinea pigs by infusing lipopolysaccharides (LPS) into the cochlea and measured the expression of Hdac2 in the sensory epithelium. We observed that the level of Hdac2 was significantly decreased in the LPS-infused cochleae. The levels of apoptosis-inhibition genes Bcl-2 and Bcl-xl were also decreased in the cochlea and correlated positively with the levels of Hdac2. Caspase3 or TUNEL-positive spiral ganglion neurons, hair cells, and supporting cells were observed in the LPS-infused cochleae. These in vivo observations were recapitulated in cell culture experiments. Based on bioinformatics analysis, we found miR-204-5p was engaged in the regulation of Hdac2 on Bcl-2. Molecular mechanism experiments displayed that miR-204-5p could be regulated by Hdac2 through interacting with transcription factor Sp1. Taken together, these results indicated that the Hdac2/Sp1/miR-204-5p/Bcl-2 regulatory axis mediated apoptosis in the cochlea, providing potential insights into the progression of acute hearing loss. To our knowledge, the study describes a miRNA-related mechanism for Hdac2-mediated regulation in the cochlea for the first time.

Differential Levels of Endoplasmic Reticulum Stress in Peripheral Blood Mononuclear Cells from Patients with Sudden Sensorineural Hearing Loss.

BACKGROUND Sudden sensorineural hearing loss (SSNHL) is currently treated with a combination of drugs, predominantly with glucocorticoids (GCs). However, the mechanisms of action of GCs in SSNHL are unknown. This study aimed to analyze the role of endoplasmic reticulum stress (ERS) in SSNHL pathogenesis and prognosis. MATERIAL AND METHODS In this study, we evaluated the expression and activation status of the protein kinase RNA-like endoplasmic reticulum kinase (PERK)-C/EBP homologous protein (CHOP) pathway in peripheral blood mononuclear cells (PBMCs) from patients with SSNHL and compared them with those in healthy controls. We also compared differences in expression of activating transcription factor 4 (ATF4) and CHOP before and after glucocorticoid treatment in patients with improved and unimproved SSNHL. RESULTS Treatment with GCs significantly improved hearing in 55% of patients with SSNHL. Levels of phosphorylated PERK (p-PERK) and phosphorylated eukaryotic initiation factor 2alpha were increased in PBMCs from patients with SSNHL compared with healthy controls. ATF4 and CHOP expression were also significantly elevated. After treatment, the amount of ATF4 and CHOP proteins in PBMCs in the patients whose SSNHL improved was significantly reduced compared with the levels measured before treatment in all patients with SSNHL. The expression of the ATF4 and CHOP proteins in PBMCs in the unimproved group, however, was not significantly changed relative to pretreatment levels. CONCLUSIONS ERS may play a significant role in the pathogenesis of SSNHL, and the responsiveness of the condition to GC-mediated mitigation of ERS may be one of the key factors that affect patient prognosis.

Panax notoginseng Saponins protect auditory cells against cisplatin­induced ototoxicity by inducing the AKT/Nrf2 signaling­mediated redox pathway.

Cisplatin­induced cytotoxicity, such as nephrotoxicity, neurotoxicity and ototoxicity, restricts the clinical application of this compound. Panax notoginseng Saponins (PNS) exhibit potent free radical scavenging and antioxidant activity. PNS have been demonstrated to reduce cisplatin­induced nephrotoxicity and neurotoxicity. The present study investigated the ability of PNS to protect the auditory HEI­OC1 cell line against ototoxicity induced by cisplatin. PNS induced activation of the AKT/nuclear factor erythroid 2­related factor 2 (Nrf2) signaling pathway. Following pretreatment with PNS, HEI­OC1 cells were treated with cisplatin and cultured for 24 h. The viability of HEI­OC1 cells was examined using a Cell Counting Kit­8 assay. Double staining analysis was used to measure cell apoptosis. The ability of PNS to reduce reactive oxygen species (ROS) levels was assessed by flow cytometry. The levels of phosphorylated (p)­AKT, heme oxygenase 1 (HO­1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutamate­cysteine ligase catalytic (GCLC) and Nrf2 were measured by western blotting. HEI­OC1 cells that were pretreated with PNS exhibited significantly increased cell viability compared with that noted in cells treated only with cisplatin. In addition, PNS suppressed the induction of apoptosis and ROS production following cisplatin treatment. The upregulation of NQO1, HO­1 and GCLC expression in PNS­pretreated cells was associated with p­AKT levels and the activation of Nrf2. These findings suggested that PNS protected auditory cells against ototoxicity induced by cisplatin by activating AKT/Nrf2 signaling. PNS may serve as a potential candidate in regulating cisplatin­induced cytotoxicity.

Correlations of MIF polymorphism and serum levels of MIF with glucocorticoid sensitivity of sudden sensorineural hearing loss.

OBJECTIVE: This study explored the relationship between macrophage migration inhibitory factor (MIF) gene polymorphism (-173G/C) and glucocorticoid sensitivity in sudden sensorineural hearing loss (SSNHL). METHODS: A total of 120 patients with SSNHL were divided into a glucocorticoid-sensitive group and a glucocorticoid-resistant group. A group of 93 healthy individuals served as the control group. Serum MIF levels of the participants were measured and MIF genotyping was performed. RESULTS: The frequency of the MIF -173C allele was significantly higher in glucocorticoid-sensitive patients than in glucocorticoid-resistant patients. Serum MIF levels were significantly higher in SSNHL patients than in healthy controls, and higher in the glucocorticoid-sensitive group than in the glucocorticoid-resistant group of SSNHL patients, which was unexpected. Compared with patients with the GG genotype, patients with the -173C allele (GC and CC genotypes) had significantly higher levels of serum MIF and superoxide dismutase activity and lower levels of tumor necrosis factor-α and malondialdehyde. CONCLUSION: The MIF -173G/C polymorphism is associated with glucocorticoid sensitivity in SSNHL patients. The C allele can result in higher MIF production, reduced oxidative stress, and greater glucocorticoid sensitivity.

Increased expression of lncRNA SNHG12 predicts a poor prognosis of nasopharyngeal carcinoma and regulates cell proliferation and metastasis by modulating Notch signal pathway.

BACKGROUND: Small nucleolar RNA host gene 12 (SNHG12) has been shown to be a long noncoding RNA (lncRNA) that facilitates the progression of a number of malignancies. However, the expression pattern and biological function of SNHG12 in nasopharyngeal carcinoma (NPC) have not been investigated. OBJECTIVE: The aim of our study is to investigate the expression, clinical significance and function of SNHG12 in NPC. METHODS: RT-PCR was used to detect the expression of SNHG12 in NPC cell lines and primary tumor tissues. The correlation of SNHG12 with clinicopathological features and patient prognosis was analyzed. The biologic functions of SNHG12 in NPC were explored by MTT assay, colony formation assay, wound healing assays, transwell assay and flow cytometric analysis in vitro. The expression of EMT markers and Notch signal pathway markers were determined by western blotting. RESULTS: The expression levels of SNHG12 were up-regulated in both NPC tissues and cell lines. High SNHG12 expression was significantly associated with clinical stage, grade and poor prognosis. Multivariate analysis demonstrated that high lncRNA SNHG12 expression was an independent poor prognostic factor for NPC patients. Functionally, knockdown of SNHG12 suppressed NPC cells proliferation, migration and invasion. Mechanistic investigations showed that knockdown of SNHG12 suppressed the activation of EMT and Notch-1 signal pathway. CONCLUSIONS: Our data suggest that SNHG12 promotes the progression of NPC and is a potential therapeutic target for NPC intervention.

MIF protects against oxygen-glucose deprivation-induced ototoxicity in HEI-OC1 cochlear cells by enhancement of Akt-Nrf2-HO-1 pathway.

Ischemia and oxidative stress play crucial roles in the pathophysiology of sudden sensorineural hearing loss (SSNHL). Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine and serves an important role in hearing function. The present study was designed to evaluate the effect of MIF on oxygen-glucose deprivation (OGD)-induced ototoxicity and to elucidate its molecular mechanism. In HEI-OC1 auditory cells, OGD reduced cell viability and increased supernatant lactate dehydrogenase (LDH) and MIF in a time-dependent manner. However, the reduced cell viability exerted by OGD was attenuated by antioxidant and MIF. Luciferase reporter assay demonstrated that MIF could activate NF-E2-related factor 2 (Nrf2), and real-time PCR showed increased mRNA expressions of Nrf2 and two Nrf2-responsive genes, including heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). MIF also suppressed oxidative stress induced by OGD, as demonstrated by decreased MDA and increased GSH in cellular supernatant. Inhibition of Nrf2 using siRNA suppressed HO-1 protein expression, the protective effect on OGD-induced injury and decrease in oxidative stress by MIF. Moreover, MIF prevented OGD-induced reduction of Akt1 phosphorylation at Ser473. LY294002, an inhibitor of PI3K/Akt signaling, attenuated the enhancement of Nrf2 protein and protective effect of MIF in OGD-treated cochlear cells. We demonstrate that MIF protects cochlear cells against OGD-induced injury through activation of Akt-Nrf2-HO-1 pathway.

Folic acid inhibits nasopharyngeal cancer cell proliferation and invasion via activation of FRα/ERK1/2/TSLC1 pathway.

Folic acid (FA), which is necessary for normal cell division of mammals, has been implicated to be involved in many tumors. Dietary FA intake has been reported to be associated with a lower risk of nasopharyngeal cancer (NPC). However, the molecular mechanisms of FA in NPC cells remain unclear. In the present study, we found that FA treatment dose dependently inhibited the proliferation, invasion and migration of NPC cells, via folate receptor α (FRα). We further found that FA, bound to FRα, induced the activation of MEK/ERK1/2, and increased the expressions of TSLC1 and E-cadherin. Moreover, blocking of ERK1/2 activation attenuated FA-mediated increase in TSLC1 expression. In addition, knockdown of TSLC1 abolished the FA-mediated inhibition of cell proliferation, invasion and migration, and suppressed the FA-mediated increase oinE-cadherin expression in NPC cells. Taken together, our data suggest that FA treatment inhibits NPC cell proliferation and invasion via activation of FRα/ERK1/2/ TSLC1 signaling pathway. Therefore, FA could be explored as a therapeutic drug for the treatment of NPC, and TSLC1 may act as a tumor suppressor in NPC.

[The expression and clinical significance of hyaluronan synthase in nasal polyps].

OBJECTIVE: To study the expression of hyaluronan synthasel-3 (HAS1-3) in nasal polyps, and discuss their clinical significance. METHOD: The expression of HA, HAS1, HAS2 and HAS3 in nasal polyps group (25 cases) and inferior turbinate group (15 cases) was detected by immunohistochemistry and semi-quantitative RT-PCR. RESULT: Compared with the control, the expression of HA, HAS1 and HAS3 was higher in nasal polyps (P<0. 05), while there was no significant difference in HAS2 expression (P>0. 05). CONCLUSION: The increase of HASI and HAS3 expression may be the main cause of the excessive deposition of HA in nasal polyps, which may play an important role in the pathogenic process of nasal polyps, and become a potential target for therapy of nasal polyps.

[Efficacy analysis of sequential surgery after the DCF scheme induction chemotherapy in T2-3 laryngeal carcinoma and hypopharyngeal carcinoma].

OBJECTIVE: To study clinical efficacy of surgery after the DCF induction chemotherapy in T2-3 laryngeal carcinoma and hypopharyngeal carcinoma. METHOD: To analyze clinical data about 102 cases of T2-3 laryngeal carcinoma and hypopharyngeal carcinoma retrospectively, 62 cases were divided into experimental group and 40 cases in control group, the experimental group completed three cycles of the DCF induction chemotherapy, then the efficacy was evaluated, surgery were carried out in the end, the control group received operation directly. In two groups, tumor response rates, toxicities, positive surgical margin rates and survival rate differences were observed and compared. RESULT: Tumor response rate was 61.3% in experimental group, the laryngeal carcinoma rate was significantly lower than that in hypopharyngeal (44.4% VS 84.6%, P < 0.05). Compared to its control, there were no significant differences about the positive surgical margin rate, the median survival time, 3-year and 5-year survival rate of laryngeal carcinoma(P > 0.05). The foci edges of 0. 3 cm and 0. 5 cm positive margin rate of hypopharyngeal carcinoma in experimental group were significantly lower than in its control (P < 0.05), but among the 1 cm edge' positive rate, the median survival time, 3-year and 5-year survival rate no significant differences were found (P > 0.05). During induction chemotherapy in the experimental group, no serious adverse reactions were found. CONCLUSION: Induction chemotherapy of DCF regimen can not only narrow T2-3 laryngeal carcinoma and hypopharyngeal carcinoma' area, but also ensure an adequate safety margin.