Thermal Oxidative Aging and Service Life Prediction of Commercial Ethylene-Propylene-Diene Monomer Spacer Damping Composites for High-Voltage Transmission Lines.

The aging behavior and life prediction of rubber composites are crucial for ensuring high-voltage transmission line safety. In this study, commercially available ethylene-propylene-diene monomer (EPDM) spacer composites were chosen and investigated to elucidate the structure and performance changes under various aging conditions. The results showed an increased C=O peak intensity with increasing aging time, suggesting intensified oxidation of ethylene and propylene units. Furthermore, the surface morphology of commercial EPDM composites displayed increased roughness and aggregation after aging. Furthermore, hardness, modulus at 100% elongation, and tensile strength of commercial EPDM composites exhibited a general increase, while elongation at break decreased. Additionally, the damping performance decreased significantly after aging, with a 20.6% reduction in loss factor (20 °C) after aging at 100 °C for 672 h. With increasing aging time and temperature, the compression set gradually rose due to the irreversible movement of the rubber chains under stress. A life prediction model was developed based on a compression set to estimate the lifetime of rubber composites for spacer bars. The results showed that the product's life was 8.4 years at 20 °C. Therefore, the establishment of a life prediction model for rubber composites can provide valuable technical support for spacer product services.

m6A-dependent upregulation of DDX21 by super-enhancer-driven IGF2BP2 and IGF2BP3 facilitates progression of acute myeloid leukaemia.

BACKGROUND: Acute myeloid leukaemia (AML) is a haematological malignancy with unfavourable prognosis. Despite the effectiveness of chemotherapy and targeted therapy, relapse or drug resistance remains a major threat to AML patients. N6-methyladenosine (m6A) RNA methylation and super-enhancers (SEs) are extensively involved in the leukaemogenesis of AML. However, the potential relationship between m6A and SEs in AML has not been elaborated. METHODS: Chromatin immunoprecipitation (ChIP) sequencing data from Gene Expression Omnibus (GEO) cohort were analysed to search SE-related genes. The mechanisms of m6 A-binding proteins IGF2BP2 and IGF2BP3 on DDX21 were explored via methylated RNA immunoprecipitation (MeRIP) assays, RNA immunoprecipitation (RIP) assays and luciferase reporter assays. Then we elucidated the roles of DDX21 in AML through functional assays in vitro and in vivo. Finally, co-immunoprecipitation (Co-IP) assays, RNA sequencing and ChIP assays were performed to investigate the downstream mechanisms of DDX21. RESULTS: We identified two SE-associated transcripts IGF2BP2 and IGF2BP3 in AML. High enrichment of H3K27ac, H3K4me1 and BRD4 was observed in IGF2BP2 and IGF2BP3, whose expression were driven by SE machinery. Then IGF2BP2 and IGF2BP3 enhanced the stability of DDX21 mRNA in an m6A-dependent manner. DDX21 was highly expressed in AML patients, which indicated a poor survival. Functionally, knockdown of DDX21 inhibited cell proliferation, promoted cell apoptosis and led to cell cycle arrest. Mechanistically, DDX21 recruited transcription factor YBX1 to cooperatively trigger ULK1 expression. Moreover, silencing of ULK1 could reverse the promoting effects of DDX21 overexpression in AML cells. CONCLUSIONS: Dysregulation of SE-IGF2BP2/IGF2BP3-DDX21 axis facilitated the progression of AML. Our findings provide new insights into the link between SEs and m6A modification, elucidate the regulatory mechanisms of IGF2BP2 and IGF2BP3 on DDX21, and reveal the underlying roles of DDX21 in AML.

BCLAF1 is Expressed as a Potential Anti-oncogene in Bile Duct Cancer.

Validating the role of BCLAF1 in the development of Bile Duct Cancer. Differential expression of BCLAF1 in Bile Duct Cancer and normal tissues was analyzed bioinformatically, and immuno-infiltration analysis was performed by R. We also derived the correlation between the expression of BCLAF1 and HIF-1α by bioinformatics analysis and validated it by Western Blotting, qRT-PCR and scratch assays before and after hypoxia. Through bioinformatics analysis, we found that BCLAF1 mRNA was significantly higher in the tumor tissues of Bile Duct Cancer. The high expression of BCLAF1 implied a more advanced stage but a lower mortality rate. KEGG and GO enrichment analysis showed that BCLAF1 overexpression in Bile Duct Cancer was mainly associated with histone modification, peptidyl lysine modification, and macromolecular methylation. We used the TIMER algorithm to show that BCLAF1 expression in Bile Duct Cancer is associated with immune cell infiltration, which affects tumor progression and patient prognosis. We confirmed by normoxia and hypoxia qRT-PCR, Western Blotting and scratch assays that BCLAF1 and HIF-1α expression are positively correlated and that BCLAF1 may be expressed as anti-oncogene in Bile Duct Cancer. These findings demonstrate that BCLAF1 may act as anti-oncogene in Bile Duct Cancer and may be involved in immune cell infiltration in Bile Duct Cancer, suppressing the expression of HIF-1α.

Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML.

KMT2A-rearranged acute myeloid leukemia (KMT2Ar-AML) is an aggressive subtype of AML with poor response and prognosis. KMT2Ar-AML has been demonstrated to be sensitive to BCL2 inhibitor venetoclax (VEN), but these patients are unable to benefit from current VEN-based regimen (VEN plus azacitidine or low dose-cytarabine), so a novel and KMT2A rearrangement-specific targeting partner is required, and MENIN inhibitor (MEN1i) is a promising one. Herein, we investigated the effect and mechanism of VEN plus MEN1i in KMT2Ar-AML. Our results showed that VEN and MEN1i exhibited a striking synergistic effect in KMT2Ar-AML cell lines (in vitro), primary KMT2Ar-AML cells (ex vivo), and MOLM13 xenotransplantation model (in vivo). Furthermore, we found that VEN plus MEN1i significantly enhanced apoptotic induction in KMT2Ar-AML cell lines. VEN or MEN1i monotherapy disrupted balance of BCL-2/BCL-XL or down-regulated HOXA9/MEIS1, respectively, but these mechanisms were not further strengthened by their combination. RNA-Sequencing identified that HDAC9 was specifically repressed by VEN plus MEN1i rather than monotherapy. We demonstrated that HDAC9 was indispensable for KMT2Ar-AML proliferation and its repression contributed to proliferation inhibition of VEN plus MEN1i. Moreover, we found that hypoxia induced HDAC9 expression in KMT2Ar-AML, and VEN plus MEN1i inhibited hypoxia pathway, especially HIF-1A, and its target HDAC9. As our results indicated, VEN plus MEN1i-mediated HDAC9 down-regulation was partially dependent on HIF-1A repression in KMT2Ar-AML. Hypoxia induction sensitized KMT2Ar-AML to VEN plus MI-503-mediated proliferation inhibition and apoptosis induction. Therefore, repressing HIF-1A-induced HDAC9 contributed to the synergistic effect of VEN and MEN1i in KMT2Ar-AML.

Determination of key factors affecting biofilm formation on the aged Poly(ethylene terephthalate) during anaerobic digestion.

Biofilm formation on plastic surface is a growing concern because it can alter the plastic surface properties and exacerbate the ecological risk. Identifying key factors that affecting biofilm formation is critical for effective pollution control. In this study, the poly (ethylene terephthalate) (PET) was aged in water and air conditions with UV irradiation, then incubated in the digestate of food waste anaerobic digestion to allow biofilm formation. Surface analysis techniques, including scanning electron microscopy (SEM), atomic force microscopy (AFM), and Fourier-transform infrared spectroscopy with attenuated total reflection (FTIR-ATR), were utilized to investigated the changes in the topography, roughness, hydrophily, and functional groups change of the PET surface during the aging process. Confocal laser scanning microscopy (CLSM) was used to determine the distribution of microorganisms on the PET surface after incubation in the digestate. This study focused on understanding the interactions between the PET surface and biofilm to identify critical surface factors that affect biofilm formation. Results showed that the four months aging process decreased the contact angle of the PET surface from 96.92° to 76.08° and 68.97° in water and air conditions, respectively, corresponding to an increase of 44% and 70% in the surface energy. Additionally, aging in air conditions led to a rougher surface compared to water conditions. The arithmetic roughness average (Ra) of the PET-Water was 11.0 nm, comparable to that of the pristine PET, while the value of PET-Air was much higher (43.9 nm). The results further indicated that biofilm formation during anaerobic digestion was more sensitive to roughness than hydrophily. The PET surface aged in air conditions provided a more suitable environment for microbial reproduction, leading to the aggradation of living cells.

Silencing of peroxiredoxin III inhibits formaldehyde-induced oxidative damage of bone marrow cells in BALB/c mice.

BACKGROUND: Formaldehyde (FA) is associated with the occurrence of leukemia, and oxidative stress is considered to be a major reason. As an endogenous biomarker of oxidative stress, few studies focus on the relationship between peroxiredoxin III (PrxIII) and FA toxicity. Our previous research observed high expression of PrxIII occurred in the process of apoptosis of bone marrow cells (BMCs) induced by FA, however the exact mechanism is unclear. Therefore, this paper aimed to explore the possible association between FA toxicity and PrxIII gene. METHODS: We first, used a Cell Counting Kit-8 (CCK-8) to detect the viability of BMCs after they were exposed to different doses of FA (50, 100, 200 µmol/L) for different exposure time (12, 24, 48 h), then chose 24 h as an exposure time to detect the expression of PrxIII for exposing different doses of FA by Quantitative reverse transcription-PCR (qRT-PCR) and Western blot analysis. Based on our preliminary experimental results, we chose 100 µmol/L FA as an exposure dose to expose for 24 h, and used a small interfering RNA (siRNA) to silenced PrxIII to examine the cell viability by CCK-8, reactive oxygen species (ROS) level by DCFH-DA, apoptosis by Annexin V/PI double staining and cell cycle by flow cytometry (FCM) so as to explore the possible regulatory effect of PrxIII silencing on FA-induced bone marrow toxicity. RESULTS: High expression of PrxIII occurred in the process of FA-induced oxidative stress. Silencing of PrxIII prevented FA from inducing oxidative stress, thus increasing cell viability, decreasing ROS level, rescuing G0 -G1 and G2 -M arrest, and reducing cell apoptosis. CONCLUSION: PrxIII silencing might be a potential target for alleviating FA-induced oxidative damage.

circSLC25A13 acts as a ceRNA to regulate AML progression via miR-616-3p/ADCY2 axis.

Circular RNAs (circRNAs), a type of endogenous noncoding RNA (ncRNA), exert vital roles in leukemia progression and are promising prognostic factors. Here, we report a novel circRNA, circSLC25A13 (hsa_circ_0081188), which was increased in acute myeloid leukemia (AML) patients with poor overall survival (OS) comparing to patients with good prognosis. Knockdown of circSLC25A13 in AML cells inhibited proliferation and increased cell apoptosis in vitro and in vivo. Enhanced circSLC25A13 expression promoted the survival of AML cells. Mechanistically, circSLC25A13 played as a microRNA sponge of miR-616-3p, which inhibited the expression of adenylate cyclase 2 (ADCY2). Downregulation of miR-616-3p and overexpression of ADCY2 partially rescued circSLC25A13 deficient induced cell growth arrest. In summary, through competitive absorption of miR-616-3p and thereby upregulating ADCY2 expression, circSLC25A13 promoted AML progression. Moreover, circSLC25A13 may represent a potential novel biomarker for the prognosis of AML and offer a potential therapeutic target for AML treatment.

Non-Invasive Detection, Precise Localization, and Perioperative Navigation of In Vivo Deep Lesions Using Transmission Raman Spectroscopy.

Non-invasive detection and precise localization of deep lesions have attracted significant attention for both fundamental and clinical studies. Optical modality techniques are promising with high sensitivity and molecular specificity, but are limited by shallow tissue penetration and the failure to accurately determine lesion depth. Here the authors report in vivo ratiometric surface-enhanced transmission Raman spectroscopy (SETRS) for non-invasive localization and perioperative surgery navigation of deep sentinel lymph nodes in live rats. The SETRS system uses ultrabright surface-enhanced Raman spectroscopy (SERS) nanoparticles with a low detection limit of 10 pM and a home-built photosafe transmission Raman spectroscopy setup. The ratiometric SETRS strategy is proposed based on the ratio of multiple Raman spectral peaks for obtaining lesion depth. Via this strategy, the depth of the phantom lesions in ex vivo rat tissues is precisely determined with a mean-absolute-percentage-error of 11.8%, and the accurate localization of a 6-mm-deep rat popliteal lymph node is achieved. The feasibility of ratiometric SETRS allows the successful perioperative navigation of in vivo lymph node biopsy surgery in live rats under clinically safe laser irradiance. This study represents a significant step toward the clinical translation of TRS techniques, providing new insights for the design and implementation of in vivo SERS applications.

PD-1+ IFN-γ+ subset of CD8+ T cell in circulation predicts response to anti-PD-1 therapy in NSCLC.

Background: Treatment with programmed cell death protein-1 (PD-1) antibodies has minimal response rates in patients with non-small cell lung cancer (NSCLC), and, actually, they are treated with chemotherapy combined with anti-PD-1 therapy clinically. Reliable markers based on circulating immune cell subsets to predict curative effect are still scarce. Methods: We included 30 patients with NSCLC treated with nivolumab or atezolizumab plus platinum drugs between 2021 and 2022. Whole blood was collected at baseline (before treatment with nivolumab or atezolizumab). The percentage of circulating PD-1+ Interferon-γ (IFN-γ+) subset of CD8+ T cell was determined by flow cytometry. The proportion of PD-1+ IFN-γ+ was calculated after gating on CD8+ T cells. Neutrophil/lymphocyte ratio (NLR), relative eosinophil count (%), and Lactate dehydrogenase (LDH) concentration at baseline of included patients were extracted from electronic medical records. Results: The percentage of circulating PD-1+ IFN-γ+ subset of CD8+ T cell at baseline in responders was significantly higher than those in non-responders (P < 0.05). Relative eosinophil count (%) and LDH concentration in responders showed no significance between non-responders and responders. NLR in responders was significantly lower than those in non-responders (P < 0.05). Receiver operation characteristic (ROC) analysis found that the areas under the ROC curve for PD-1+ IFN-γ+ subset of CD8+ T cell and NLR were 0.7781 (95% CI, 0.5937-0.9526) and 0.7315 (95% CI, 0.5169-0.9461). Moreover, high percentage of PD-1+ IFN-γ+ subset in CD8+ T cells was relevant to long progression-free survival in patients with NSCLC treated with chemotherapy combined with anti-PD-1 therapy. Conclusion: The percentage of circulating PD-1+ IFN-γ+ subset of CD8+ T cell could be a potential marker at baseline to predict early response or progression in patients with NSCLC receiving chemotherapy combined with anti-PD-1 therapy.

Glutamate dehydrogenase 1: A novel metabolic target in inhibiting acute myeloid leukaemia progression.

Glutamine metabolic reprogramming in acute myeloid leukaemia (AML) cells contributes to the decreased sensitivity to antileukemic drugs. Leukaemic cells, but not their myeloid counterparts, largely depend on glutamine. Glutamate dehydrogenase 1 (GDH1) is a regulation enzyme in glutaminolysis. However, its role in AML remains unknown. Here, we reported that GDH1 was highly expressed in AML: high GDH1 was one of the independent negative prognostic factors in AML cohort. The dependence of leukaemic cells on GDH1 was proved both in vitro and in vivo. High GDH1 promoted cell proliferation and reduced survival time of leukaemic mice. Targeting GDH1 eliminated the blast cells and delayed AML progression. Mechanistically, GDH1 knockdown inhibited glutamine uptake by downregulating SLC1A5. Moreover, GDH1 invalidation also inhibited SLC3A2 and abrogated the cystine-glutamate antiporter system Xc- . The reduced cystine and glutamine disrupted the synthesis of glutathione (GSH) and led to the dysfunction of glutathione peroxidase-4 (GPX4), which maintains the lipid peroxidation homeostasis by using GSH as a co-factor. Collectively, triggering ferroptosis in AML cells in a GSH depletion manner, GDH1 inhibition was synthetically lethal with the chemotherapy drug cytarabine. Ferroptosis induced by inhibiting GDH1 provides an actionable therapeutic opportunity and a unique target for synthetic lethality to facilitate the elimination of malignant AML cells.

Pharmacological mechanism of natural drugs and their active ingredients in the treatment of arrhythmia via calcium channel regulation.

Arrhythmia is characterized by abnormal heartbeat rhythms and frequencies caused by heart pacing and conduction dysfunction. Arrhythmia is the leading cause of death in patients with cardiovascular disease, with high morbidity and mortality rates, posing a serious risk to human health. Natural drugs and their active ingredients, such as matrine(MAT), tetrandrine(TET), dehydroevodiamine, tanshinone IIA, and ginsenosides, have been widely used for the treatment of atrial fibrillation, ventricular ectopic beats, sick sinus syndrome, and other arrhythmia-like diseases owing to their unique advantages. This review summarizes the mechanism of action of natural drugs and their active ingredients in the treatment of arrhythmia via the regulation of Ca2+, such as alkaloids, quinones, saponins, terpenoids, flavonoids, polyphenols, and lignan compounds, to provide ideas for the innovative development of natural drugs with potential antiarrhythmic efficacy.

The changed endemic pattern of human adenovirus from species B to C among pediatric patients under the pressure of non-pharmaceutical interventions against COVID-19 in Beijing, China.

BACKGROUND: Under the pressure of non-pharmaceutical interventions (NPIs) targeting severe acute respiratory syndrome coronavirus 2, the prevalence of human adenovirus (HAdV) was monitored before and after NPIs launched on Jan 24, 2020 in pediatric patients in Beijing, China. METHODS: Respiratory samples collected from children hospitalized with acute respiratory infections from Jan 2015 to Dec 2021 were screened by direct immunofluorescence test or capillary electrophoresis-based multiplex PCR assay. The hexon, penton base, and fiber genes were amplified from HAdV positive specimens, then sequenced. For HAdV typing, phylogenetic trees were built by MEGA X. Then clinical data of HAdV positive cases were collected. All data were evaluated using SPSS Statistics 22.0 software. RESULTS: A total of 16,097 children were enrolled and 466 (2.89%, 466/16,097) were HAdV-positive. The positive rates of HAdV varied, ranging from 4.39% (151/3,438) in 2018 to1.25% (26/2,081) in 2021, dropped from 3.19% (428/13,408) to 1.41% (38/2,689) from before to after NPIs launched (P < 0.001). There were 350 cases typed into nine types of species B, C, or E and 34 recorded as undetermined. Among them, HAdV-B3 (51.56%, 198/384) was the most prevalent types from 2015 to 2017, and HAdV-B7 (29.17%, 112/384) co-circulated with HAdV-B3 from 2018 to 2019. After NPIs launched, HAdV-B3 and B7 decreased sharply with HAdV-B7 undetected in 2021, while HAdV-C1 became the dominant one and the undetermined were more. CONCLUSIONS: The endemic pattern of HAdV changed in Beijing because of the NPIs launched for COVID-19. Especially, the dominant types changed from HAdV-B to HAdV-C.

FLOT1 knockdown inhibits growth of AML cells through triggering apoptosis and pyroptosis.

Acute myeloid leukemia (AML) is a group of hematological malignancies characterized by clonal proliferation of immature myeloid cells. Lipid rafts are highly organized membrane subdomains enriched in cholesterol, sphingolipids, and gangliosides and play roles in regulating apoptosis through subcellular redistribution. Flotillin1 (FLOT1) is a component and also a marker of lipid rafts and had been reported to be involved in the progression of cancers and played important roles in cell death. However, the role of FLOT1 in AML remains to be explored. In this study, we found that increased expression of FLOT1 was correlated with poor clinical outcome in AML patients. Knockdown of FLOT1 in AML cells not only promoted cell death in vitro but also inhibited malignant cells engraftment in vivo. Mechanically, FLOT1 knockdown triggered apoptosis and pyroptosis. FLOT1 overexpression promoted AML cell growth and apoptosis resistance. Our findings indicate that FLOT1 is a prognostic factor of AML and may be a potential target for AML treatment.

ACC010, a novel BRD4 inhibitor, synergized with homoharringtonine in acute myeloid leukemia with FLT3-ITD.

Bromodomain-containing protein 4 (BRD4) inhibitors have been clinically developed to treat acute myeloid leukemia (AML), but their application is limited by the possibility of drug resistance, which is reportedly associated with the activation of the WNT/ß-catenin pathway. Meanwhile, homoharringtonine (HHT), a classic antileukemia drug, possibly inhibits the WNT/ß-catenin pathway. In this study, we attempted to combine a novel BRD4 inhibitor (ACC010) and HHT to explore their synergistic lethal effects in treating AML. Here, we found that co-treatment with ACC010 and HHT synergistically inhibited cell proliferation, induced apoptosis, and arrested the cell cycle in FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD)-positive AML cells in vitro, and significantly inhibiting AML progression in vivo. Mechanistically, ACC010 and HHT cooperatively downregulated MYC and inhibited FLT3 activation. Further, when HHT was added, ACC010-resistant cells demonstrated a good synergy. We also extended our study to the mouse BaF3 cell line with FLT3-inhibitor-resistant FLT3-ITD/tyrosine kinase domain mutations and AML cells without FLT3-ITD. Collectively, our results suggested that the combination treatment of ACC010 and HHT might be a promising strategy for AML patients, especially those carrying FLT3-ITD.

Taxifolin attenuates inflammation via suppressing MAPK signal pathway in vitro and in silico analysis.

Objective: Taxifolin is a natural flavonoid compound that can be isolated from onions, grapes, oranges and grapefruit. It also acts as a medicine food homology with extraordinary antioxidant and anti-inflammatory activity. This study aims to explain the protective effects and potential mechanisms of taxifolin against inflammatory reaction. Methods: Levels of interleukin (IL)-6, IL-1ß and intracellular reactive oxygen species (ROS) were assessed in different time after the treatment of taxifolin in RAW264.7 cells induced by lipopolysaccharide (LPS). Subsequently, the mRNA and protein levels of inducible nitric oxide synthase (iNOS), vascular endothelial growth factor (VEGF), cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-α and the phosphorylation expression levels of the MAPK signal pathway were also evaluated. A silico analysis was used to explain the binding situation for the investigation of taxifolin and MAPK signal pathway. And then MAPK inhibitors were used to reveal the expression level of iNOS, VEGF, COX-2 and TNF-α in RAW264.7 cells. Results: It was demonstrated that cell inflammatory damage induced by LPS was significantly alleviated after the treatment of taxifolin. Then, the mRNA and protein levels of iNOS, VEGF, COX-2 and TNF-α were reduced and the phosphorylation expression levels of the MAPK signal pathway were down-regulated remarkably as well. In silico analysis, taxifolin could form a relatively stable combination with MAPK signal pathway. MAPK inhibitors showed increasing or decreasing effect in the mRNA levels of iNOS, VEGF, COX-2 and TNF-α, which suggesting that taxifolin down-regulated iNOS, VEGF, COX-2 and TNF-α expressions were not entirely through the MAPK pathway. Conclusion: This finding demonstrated that taxifolin improved the inflammatory responses that partly involved in the phosphorylation expression level of MAPK signal pathway in RAW264.7 cells exposed to acute stress.

[Effects of age and involved semicircular canals on the caloric test in patients with primary horizontal semicircular canal benign paroxysmal positional vertigo].

Objective:To investigate the effects of age and involved semicircular canals on the results of caloric test in patients with primary horizontal semicircular canal benign paroxysmal positional vertigo（BPPV）. Methods:A total of 258 patients conforming to the diagnosis of primary horizontal semicircular canal BPPV were selected as the case group, and another 110 non-BPPV patients with dizziness/vertigo as the main complaint were selected as the control group. Both groups were divided into elderly group and young and middle-aged group according to their age, and the general information and the results of the caloric test were compared and analyzed for each group. Results: ①There was no statistically significant difference in gender composition and type of involved semicircular canal between the different age groups（P>0.05）；②In patients with horizontal semicircular canal canalolithiasis, there was no statistically significant difference in the rate of abnormal caloric test results between the different age groups（P>0.05）；③In patients with horizontal semicircular canal cupulolithiasis, there was a statistically significant difference in the rate of abnormal caloric test results between the different age groups（P<0.05）；④In the same age group, there was no statistically significant difference in the rate of abnormal caloric test results between the patients with horizontal semicircular canal canalolithiasis and the patients with cupulolithiasis（P>0.05）；⑤In the control group, there was no statistically significant difference between the different age groups in gender composition（P>0.05）；⑥In the control group, there was a statistically significant difference in the rate of abnormal caloric test results between the different age groups（P<0.05）；⑦Among the patients in the same age group, there was no statistically significant difference in the age distribution between the case and control groups（P>0.05）；⑧In patients of the same age group, there was no statistically significant difference in the rate of abnormal caloric test results between the case and control groups（P>0.05）. Conclusion:The involvement of the semicircular canal does not affect the results of the caloric test, but age can affect the results, especially in BPPV patients with horizontal semicircular canal cupulolithiasis.

Roles and mechanisms of quercetin on cardiac arrhythmia: A review.

Cardiac arrhythmia is one of the most prevalent cardiovascular diseases worldwide, which can occur alone or be triggered by other diseases, and it can be fatal in severe cases. Recently, Traditional Chinese Medicine has drawn the world's attention to its effective treatment. As a natural polyhydroxy flavonoid mainly isolated from a variety of plants and foods, quercetin is used for the treatment of cardiovascular disease, cancer, autoimmune diseases, and neurological disorders. A growing number of in vitro experiments and in vivo animal studies have shown that quercetin significantly inhibits mitochondrial oxidative stress, cardiac fibrosis, inflammatory responses, and apoptosis, regulates autophagic responses, improves ischemia/reperfusion injury in cardiomyocytes, and regulates gut microbiota, thereby attenuating or preventing structural and electrical remodeling in the cardiac. Based on these mechanisms, our review provides a systematic overview of the pharmacological actions and molecular targets of quercetin in cardiac arrhythmia caused by multiple etiologies, aiming to provide novel insights and therapeutic strategies to prevent or ameliorate arrhythmia.

Surges of hospital-based rhinovirus infection during the 2020 coronavirus disease-19 (COVID-19) pandemic in Beijing, China.

BACKGROUND: A series of public health preventive measures has been widely implemented in Beijing to control the coronavirus disease-19 (COVID-19) pandemic since January 2020. An evaluation of the effects of these preventive measures on the spread of other respiratory viruses is necessary. METHODS: Respiratory specimens collected from children with acute respiratory infections were tested by NxTAG™ respiratory pathogen panel assays during January 2017 and December 2020. Specimens characterized as rhinoviruses (RVs) were sequenced to identify the RV species and types. Then, the epidemiology results of respiratory pathogens in 2020 were compared with those from 2017 to 2019 using SPSS statistics 22.0. RESULTS: The positive rates of adenovirus (ADV), influenza virus (flu), RVs, and respiratory syncytial virus (RSV) dropped abruptly by 86.31%, 94.67%, 94.59%, and 92.17%, respectively, from February to May 2020, compared with the average level in the same period during 2017-2019. Positive rates of RVs then steeply increased from June 2020 (13.77%), to an apex (37.25%) in August 2020, significantly higher than the average rates (22.51%) in August 2017-2019 (P = 0.005). The increase, especially in group ≥ 3 years, was accompanied by the reopening of schools and kindergartens after the 23rd and 24th week of 2020 in Beijing. CONCLUSIONS: Whereas the abrupt drop in viral pathogen positive rates from February to May 2020 revealed the remarkable effects of the COVID-19 preventive measures, the sharp increase in positive rates of RVs from the 23rd week of 2020 might be explained by the reopening of schools and kindergartens in Beijing.

Weighted genes associated with the progression of retinoblastoma: Evidence from bioinformatic analysis.

Mechanisms underlying the development of malignant retinoblastoma (RB) remain largely unknown. The purpose of this study was to identify weighted genes that are associated with the progression of RB and to assess the usefulness of bioinformatic analysis in RB research. Bioinformatic analysis was performed to construct weighted gene co-expression and protein-protein interaction (PPI) networks and to predict long non-coding RNA (lncRNA)-microRNA (miRNA)-mRNA regulatory networks. RNA extracted from RB and adjacent retinal tissue was used to validate the results obtained from bioinformatic analysis, using a semi-quantitative PCR (qPCR) assay. Twenty-one modules were generated from 5000 most variably expressed genes. Both the light-yellow and red modules were significantly associated with the cellular anaplastic grade of RB. The genes clustered in the light-yellow module included protocadherin beta (PCDHBs) family members. The red module included 5 hub genes involved in cell division. According to the hypothesis that lncRNA may serve as a competing endogenous RNA (ceRNA) for miRNAs and modulates mRNA expression, a network was constructed between lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and cell division-related mRNAs. PCR analysis using 23 tumor tissues and 5 adjacent retinal tissue showed increased expression of PCDHB5 in tumor samples, and supported the predicted upregulation of mitotic checkpoint serine/threonine kinase (BUB1) by MALAT1 via miR-495-3p. Our study highlights the importance of bioinformatic analysis in identifying potential markers and mechanisms associated with the malignant transformation of RB, and provides evidence to suggest that PCDHB5 and the ceRNA regulatory network of MALAT1/miR-495-3p/BUB1 are involved in the progression of RB.