Differences in brain functional connectivity between tinnitus with or without hearing loss.

To explore the differences in brain imaging in tinnitus with or without hearing loss (HL). We acquired functional MRI scans from 26 tinnitus patients with HL (tinnitus-HL), 24 tinnitus patients with no HL (tinnitus-NHL), and 26 healthy controls (HCs) matched by age and sex. The left and right thalamus were selected as seeds to study the endogenous functional connectivity (FC) of the whole brain, and its correlation with clinical indices was analyzed. Brain regions showing FC differences among the three groups included the Heschl gyrus (HES), right Hippocampus (HIP), right Amygdala (AMYG), left Calcarine fissure and surrounding cortex (CAL). Post hoc analysis showed that the thalamus-HIP connection and thalamus-lingual gyrus (LING) connection were enhanced in the tinnitus-NHL group, as compared to tinnitus-HL. Compared with HCs, the tinnitus-NHL group showed an enhanced connection between the thalamus and the left Inferior occipital gyrus, left CAL and LING. While in the tinnitus-HL group, the connection between the thalamus and several brain regions (right HES, right AMYG, etc) was weakened. In the tinnitus-HL group, the tinnitus handicap inventory scores were positively correlated with the FC of the left thalamus and right HES, right thalamus and right Rolandic operculum. The duration of tinnitus was negatively correlated with the FC of the right thalamus and right HIP. Abnormal FC in the thalamus may play an important role in the pathogenesis of tinnitus. Tinnitus-NHL and tinnitus-HL show different connection patterns, indicating that there are some differences in their pathogenesis.

Reassessment of oxidative stress in idiopathic sudden hearing loss and preliminary exploration of the effect of physiological concentration of melatonin on prognosis.

Background and purpose: The pathogenesis of idiopathic sudden sensorineural hearing loss (ISSNHL) is still unclear, and there is no targeted treatment. This research aimed to verify the role of oxidative stress in ISSNHL and explore whether melatonin has a protective effect on hearing. Materials and methods: A total of 43 patients with ISSNHL and 15 healthy controls were recruited to detect the level of melatonin, reactive oxygen species (ROS), and total antioxidant capacity (TAC) in the blood and compared before and after treatment. Multivariate logistic regression models were performed to assess the factors relevant to the occurrence and improvement of ISSNHL. Results: The patients with ISSNHL showed significantly higher ROS levels than controls (4.42 ± 4.40 vs. 2.30 ± 0.59; p = 0.031). The levels of basal melatonin were higher (1400.83 ± 784.89 vs. 1095.97 ± 689.08; p = 0.046) and ROS levels were lower (3.05 ± 1.81 vs. 5.62 ± 5.56; p = 0.042) in the effective group as compared with the ineffective group. Logistic regression analysis showed that melatonin (OR = 0.999, 95% CI 0.997-1.000, p = 0.049), ROS (OR = 1.154, 95% CI 1.025-2.236, p = 0.037), and vertigo (OR = 3.011, 95% CI 1.339-26.983, p = 0.019) were independent factors associated with hearing improvement. Besides, the level of melatonin (OR = 0.999, 95% CI 0.998-1.000, p = 0.023) and ROS (OR = 3.248, 95% CI 1.109-9.516, p = 0.032) were associated with the occurrence of ISSNHL. Conclusion: Our findings may suggest oxidative stress involvement in ISSNHL etiopathogenesis. The level of melatonin and ROS, and vertigo appear to be predictive of the effectiveness of hearing improvement following ISSNHL treatment.

CSMD1 Mutation Related to Immunity Can Be Used as a Marker to Evaluate the Clinical Therapeutic Effect and Prognosis of Patients with Esophageal Cancer.

INTRODUCTION: As a highly aggressive tumor with a poor prognosis, esophageal cancer (ESCA)'s relationship with gene mutations is unclear. Therefore, we tried to explore the role of gene mutation in ESCA progression and its relationship with immune response, clinical treatment, and prognosis. METHODS: In addition to copy number variation (CNV) situations of common genes obtained from 2 public databases, the relationship between mutations and prognosis/tumor mutational burden (TMB) was also analyzed. Kaplan-Meier survival and Cox regression analysis were used to identify the CSMD1 mutation status as an independent predictor of prognosis. We also enriched related functions and pathways. Next, the relationship between 22 immune cells and CSMD1 mutation status was analyzed. In addition to the differences in the expression levels of immune checkpoint inhibitors (ICIs)-related genes between the high TMB and low TMB groups, the differences in the expression levels of ICIs/m6a/multi-drug resistance-related genes and the sensitivity of three chemotherapeutic drugs between CSMD1 mutant and the wild group were also compared. In addition to differences and prognostic analysis of CSMD1 expression, the correlation analysis between the expression of these genes/immune cells and the expression of CSMD1 was also performed. Finally, a nomogram that could efficiently and conveniently predict the survival probability of ESCA patients was constructed and verified. RESULTS: We obtained 17 frequently mutated genes distribution. Mutation and loss of CSMD1 are frequent in ESCA. Only CSMD1 mutation can be used as an independent predictor of poor prognosis. Patients in the high TMB group have a lower survival probability. Wild CSMD1 may be involved in immune-related pathways. More helper T cells and fewer resting state dendritic cells were found in the CSMD1 mutant group. The PD-1 expression in the high TMB group showed higher. Paclitaxel sensitivity and ABCC1 expression were higher in the wild CSMD1 group. Most cancers show differential expression of CSMD1. Except for the prognosis of ESCA, the expression of CSMD1 is related to immune cell content and the expression of ICIs/m6a/multi-drug resistance related genes. DISCUSSION: CSMD1 mutation could be used as an immune-related biomarker to predict prognosis and treatment effect of paclitaxel. Mutation and loss of CSMD1 may promote the progression of ESCA.

[Influences of severe obstructive sleep apnea on cognitive function].

Objective:To explore the differences in cognitive function between patients with severe OSA and non-moderate OSA. Methods:The MoCA scale was used to evaluate the overall cognitive function and sub-items in 196 subjects who received polysomnography; and the SDMT and TMT-A scales were used to evaluate the performance in test of attention and information processing speed in 161 patients. The clinical information, physical examination data and related polysomnography data were collected. According to AHI, subjects were divided into two groups: severe OSA and non-to-moderate OSA. Before and after correction of confounding factors, the differences in cognitive scale evaluation indicators were compared between the two groups. We used linear regression analysis to clarify the independent influencing factors of cognitive functions, and to determine whether severe OSA is independently related to cognitive abilities. Results:After correcting for multiple factors, the delayed recall score and total score of the MoCA scale and the correct number of SDMT in the severe OSA group were significantly lower than those in the non-to-moderate OSA group（P<0.05）. Linear regression analysis showed that severe OSA was independently negatively correlated with the delayed recall score, total score and SDMT correct number in the MoCA scale（P<0.05）. Conclusion:Compared with non-to-moderate OSA, subjects with severe OSA have significant decline in overall cognition, delayed recall, attention and processing speed. Severe OSA may be an independent influencing factor of overall cognition, delayed recall, attention and processing speed.