Diagnostic value of 3D-FLAIR MRI in children with sudden deafness caused by inner ear hemorrhage.

Objective: To investigate the diagnostic value of three-dimensional fluid-attenuated inversion recovery (3D-FLAIR) MRI in children with sudden deafness caused by inner ear hemorrhage. Methods: The diagnostic efficacies of three different MRI sequences in the examination of the inner ear for 32 children with sudden deafness were compared. Hearing examination results and 3-month follow-up outcomes were analyzed. Results: The age of 32 children with sudden deafness ranged from 5 to 18 years. MRI was performed from 1 to 18 days after onset. Six cases of sudden deafness caused by inner ear hemorrhage were finally diagnosed clinically. For different MRI sequences, the 3D-FLAIR sequence detected five positive cases; the conventional T1-weighted image sequence also detected five positive cases; but the conventional T2-weighted image sequence only detected three positive cases. The sensitivity and specificity of the 3D-FLAIR sequence in the diagnosis of inner ear hemorrhage were 83.3% (5/6) and 96.2% (25/26), respectively, and the area under the curve value of the receiver operating characteristic curve was 0.897. In the hemorrhage group, all six cases had extremely severe sensorineural hearing loss, and the hearing recovery was ineffective after 3 months of follow-up. The degree of hearing impairment, 3-month short-term treatment efficacy, and 3D-FLAIR MRI in the diagnosis of inner ear hemorrhage between hemorrhage group and non-hemorrhage group were statistically significant (p=0.043, p=0.000, p=0.000). Conclusions: 3D-FLAIR MRI is helpful for the diagnosis of inner ear hemorrhage in children with sudden deafness. Besides, short-term treatment indicates poor effects on children with severe hearing impairment.

[Application of vacuum stretcher combined with feeding in cranial magnetic resonance imaging examination for neonates: a prospective randomized controlled study].

OBJECTIVE: To study the effect and safety of vacuum stretcher combined with feeding in cranial magnetic resonance imaging (MRI) examination for neonates. METHODS: A prospective study was performed for the neonates with hyperbilirubinemia, with a gestational age of >34 weeks and stable vital signs, who needed cranial MRI examination and did not need oxygen inhalation hospitalized in the Department of Neonatology, Children's Hospital of Zhejiang University School of Medicine, from September to November, 2019. The neonates were randomly divided into a vacuum stretcher combined with feeding group and a conventional sedation group. Vital signs were monitored before, during, and after MRI examination. The success rate of MRI procedure was recorded. RESULTS: A total of 80 neonates were enrolled in the study, with 40 neonates in the vacuum stretcher combined with feeding group and 40 in the conventional sedation group. The vacuum stretcher combined with feeding group had a significantly higher success rate of MRI procedure than the conventional sedation group (P<0.05). As for the neonates who underwent successful MRI examination, the fastest heart rate after examination in the vacuum stretcher combined with feeding group was significantly lower than that in the conventional sedation group (P<0.05), while there were no significant differences between the two groups in transcutaneous oxygen saturation, respiratory rate, and body temperature before and after MRI examination (P>0.05). No complications, such as apnea, acute allergic reactions, and malignant fever, were observed. CONCLUSIONS: Vacuum stretcher combined with feeding can improve the success rate of MRI procedure and reduce the use of sedatives, and meanwhile, it does not increase related risks.

Enhancement of anti-tumor effect of plasmid DNA-carrying MUC1 by the adjuvanticity of FLT3L in mouse model.

AIM: DNA vaccines have emerged as a promising strategy for cancer immunotherapy; however, their immunogenicity is weak. Fms-like tyrosine kinase 3-ligand (Flt3L) has been exploited for its ability to increase the proliferation of dendritic cells (DCs). The aim of the present study was to investigate whether co-administration of an adjuvant plasmid expressing mouse Flt3L and a DNA vaccine of the Mucin 1 (MUC1) antigen enhances immune responses. METHODS: The recombinant plasmids pVAX1-MUC1 and pVAX1-Flt3L were constructed and injected into mice intramuscularly (i.m.), followed by electroporation. The humoral and cellular immune responses after immunization were examined by enzyme linked immunosorbent assay (ELISA) and enzyme-linked immunospot assay (ELISPOT), respectively. To evaluate the anti-tumor efficacy of the plasmids, a mouse model of MUC1-expressing tumors was established. RESULTS: The results showed that co-administration of an adjuvant plasmid and a DNA vaccine stimulated the production of higher titers of specific antibodies and a T cell response and suppressed the growth of subcutaneous tumors expressing MUC1. Collectively, our results indicate that a plasmid expressing murine Flt3L could stimulate stronger immune responses. CONCLUSION: These observations emphasize the potential of Flt3L as an adjuvant for colon cancer DNA vaccines.

Effects of chronic exposure to Aspergillus fumigatus on epidermal growth factor receptor expression in the airway epithelial cells of asthmatic rats.

Epidemiologic studies suggest that increased concentrations of airborne spores of Aspergillus fumigatus closely relate to asthma aggravation. Chronic exposure to A. fumigatus aggravates airway inflammation, remodeling, and airway hyperresponsiveness in asthmatic rats. The effects of chronic exposure to A. fumigatus on epidermal growth factor receptor (EGFR) expression in the airway epithelial cells of asthmatic rats remain unclear. This study aimed to investigate the effects of chronic exposure to A. fumigatus on injury and shedding of airway epithelium, goblet cell metaplasia, and EGFR expression in the airway epithelial cells of asthmatic rats. A rat model of chronic asthma was established using ovalbumin (OVA) sensitization and challenge. Rats with chronic asthma were then exposed to long-term inhalation of spores of A. fumigatus, and the dynamic changes in injury and shedding of airway epithelium, goblet cell metaplasia, and EGFR expression were observed and analyzed. Chronic exposure to A. fumigatus could aggravate airway epithelial cell damage, upregulate the expression of EGFR and its ligands EGF and TGF-α, promote goblet cell metaplasia, and increase airway responsiveness in rats with asthma. Chronic exposure to A. fumigatus upregulates the expression of EGFR and its ligands in asthmatic rats. The EGFR pathway may play a role in asthma aggravation induced by exposure to A. fumigatus.

[Effects of chronic Aspergillus fumigatus exposure on the expression of mucin 5AC in the airways of asthmatic rats].

OBJECTIVE: To explore the effects of chronic Aspergillus fumigatus (Af) exposure on the expression of mucin 5AC (MUC5AC) in the airways of asthmatic rats. METHODS: Fifty-six male Wistar rats were randomly divided into 8 groups: chronic asthma (group A), chronic asthma plus Af spores inhalation for 1 week (group B), 3 weeks (group C) and 5 weeks (group D), chronic asthma plus saline inhalation for 5 weeks (group E), OVA-sensitized and-saline-challenged group (group F) and OVA-sensitized and-saline-challenged plus Af spores inhalation for 5 weeks (group G) (each n = 8). The airway resistance (Raw) and the change rate of Raw after acetylcholine provocation were detected using a computerized system. The level of MUC5AC mRNA in the lung tissue was measured by RT-PCR, and the expression of MUC5AC in airway epithelial cells were demonstrated by immunohistochemistry. The concentration of IL-13 in BALF was measured by ELISA. The extent of goblet cell hyperplasia was evaluated on periodic acid-Schiff stain (PAS) lung sections. RESULTS: In group B, C, and D, the level of MUC5AC mRNA (MUC5AC mRNA/ß-actin mRNA) (1.9 ± 0.4, 2.3 ± 0.6, 2.9 ± 0.8, respectively), the integrated optical density (value A) of MUC5AC positive stain in airway epithelial cells (278 ± 58, 566 ± 64, 891 ± 80, respectively), the concentration of IL-13 in BALF (µg/L) (96 ± 16, 136 ± 22, 197 ± 34, respectively), and the ratio of goblet cell area to epithelial cell area(%) (16 ± 5, 23 ± 7, 36 ± 9, respectively), were higher than those in group A, E, F and G (all P < 0.05). The change rate of Raw(%) in group C and D (61.91 ± 5.26 and 84.69 ± 6.38) were higher than that in group A, E, F and G (all P < 0.05). The level of MUC5AC mRNA and the value A of MUC5AC were positively correlated with the ratio of goblet cell area to epithelial cell area (r = 0.578, P < 0.05;r = 0.614, P < 0.05, respectively) and the change rate of Raw (r = 0.638, P < 0.05;r = 0.564, P < 0.05, respectively) in group B, C and D. CONCLUSION: Chronic Aspergillus fumigatus exposure upregulated the expression of MUC5AC in the airway epithelial cells and induced goblet cell hyperplasia, resulting in increased airway hypersensitivity in rats with chronic asthma.

Chronic Aspergillus fumigatus exposure upregulates the expression of mucin 5AC in the airways of asthmatic rats.

BACKGROUND: Airway mucus hypersecretion is associated with increased morbidity and mortality in patients with asthma. Chronic Aspergillus fumigatus (A. fumigatus) exposure leads to aggravation of airway inflammation and remodeling, including goblet cell hyperplasia (GCH) and mucus hypersecretion in a rat model of asthma. The effects of chronic A. fumigatus exposure on the expression of airway mucin 5AC (MUC5AC) are unknown. METHODS: The rat model of chronic asthma was set up by systemic sensitization and repeated challenge to ovalbumin (OVA). The asthmatic rats were exposed to chronic intranasal inhalation of A. fumigatus spores. The changes of MUC5AC expression, the extent of GCH, and airway hyperreactivity (AHR) were measured after exposure to the fungus. RESULTS AND CONCLUSIONS: Chronic exposure to A. fumigatus upregulates the expression of MUC5AC, and induces GCH in the airways of asthma rats, and the remodeling changes of the airway epithelium was positively correlated with AHR. Upregulation of MUC5AC and induction of GCH may be mechanisms by which chronic A. fumigatus exposure promotes the progression of asthma.

Chronic intranasal administration of Aspergillus fumigatus spores leads to aggravation of airway inflammation and remodelling in asthmatic rats.

BACKGROUND AND OBJECTIVE: Epidemiological evidence indicates a close link between exposure to fungi and deterioration of asthma. However, the role of fungi as an exogenous precipitant for initiation and progression of asthma has been incompletely explored. In this study, the effects of Aspergillus fumigatus exposure on airway inflammation and remodelling in a rat model of chronic asthma were investigated. METHODS: The rat model of chronic asthma was established by systemic sensitization and repeated challenge with ovalbumin (OVA). The asthmatic rats were exposed to chronic intranasal inhalation of A. fumigatus spores. Changes in airway inflammation, remodelling and BHR were measured after exposure to the fungus. RESULTS: Chronic inhalation of A. fumigatus spores elevated the production of T helper 2 (Th2) cytokines, increased the concentration of total serum IgE, and resulted in the recruitment of eosinophils and lymphocyte infiltration into the airways of asthmatic rats. Goblet cell hyperplasia, mucus hyperproduction and subepithelial collagen deposition were also induced by inhalation of the fungus. The remodelling changes induced by inhalation of the fungus paralleled the changes in BHR in this rat model of asthma. CONCLUSIONS: Chronic exposure to A. fumigatus aggravated Th2 airway inflammation, promoted airway remodelling and increased BHR in OVA-sensitized and -challenged rats.

[The changes of advanced glycation end products in a rat liver fibrosis model and the interventional effect of aminoguanidin].

OBJECTIVE: To study the changes of advanced glycation end products (AGEs) in different phases of a rat liver fibrosis model induced by CCl4, and the interventional effect of aminoguanidin (AG). METHODS: Fifty-four SD rats were divided into three groups: a control group, a CCl4 model group and an intervention group. Their blood serum AGEs and hyaluronic acid (HA) and AGEs in their liver homogenates were measured. These measurements were correlatively assessed to the degrees of liver fibrosis at different phases of the rat model before and after the intervention with aminoguanidin. RESULTS: The content of AGEs in their blood sera and liver homogenates, and the level of blood serum HA, and the score of liver fibrosis degree at week 12 in our rat liver fibrosis mode groups were significantly higher than those in the control group (P < 0.01). In the intervention group with aminoguanidin, these figures were lower than those in the liver fibrosis model group (P < 0.05). The content of AGEs in their blood sera and liver homogenates had a linear correlation with the level of HA in their blood sera. CONCLUSION: The contents of AGEs in their blood sera and liver homogenates were increased in the late phase of our rat liver fibrosis model. To some extent, the level of AGEs may reflect the fibrosis degree of the rat livers. Aminoguanidin has an interventional effect in our CCl4 induced rat liver fibrosis model.