Qing-Qing Jiang

Qing-Qing Jiang

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

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Previous Organizations / Institutes

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Qing-Qing Jiang has a total of 41 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Open Access

    CD38 Coordinates with NF-κB to Promote Cochlear Inflammation in Noise-Induced Hearing Loss: the Protective Effect of Apigenin

    by Da Liu, Na Sai, Ying Zhou, Ning Yu, Qing-Qing Jiang, Wei Sun, Wei-Ju Han, Weiwei Guo

    Noise exposure is one of the most common causes of sensorineural hearing loss. Although many studies considered inflammation to be a major contributor to noise-induced hearing loss, the process of cochlear inflammation is still unclear. Studies have found that activation of the NF-κB signaling pathway results in the accumulation of macrophages in the inner ear plays an important role in hair cell damage. In this study, tandem mass tag (TMT) technique was used to analyze the changes in basilar membrane proteome expression before and after acoustic injury. After noise exposure, the nicotinamide adenine dinucleotide (NAD) metabolism level was decreased, and the NF-κB signaling pathway was activated. The expression of CD38, the main NAD hydrolase in mammals, may directly lead to inflammation onset. Then, anakinra, an IL-1 receptor blocker, and apigenin, a CD38 inhibitor, were administered to animals to protect against noise-induced hearing loss. Our results showed that anakinra had little influence on the hearing threshold shift, while apigenin significantly reduce the threshold shift of hearing by inhibiting the expression of NF-κB and CD38 can be a promising target for protecting against noise-induced hearing loss.


  • Open Access

    Ferroptosis inhibition shields house ear institute-organ of corti 1 cells from free fatty acids-induced inflammatory injuries

    by Xuemin Chen, Yiding Yu, Ning Yu, Weiwei Guo, Qingqing Jiang, Shiming Yang

    Free fatty acids (FFAs) could induce inflammatory responses via various pathways. Ferroptosis is characterized by the accumulation of lipid peroxidation products and fatal reactive oxygen species d... 背景:游离脂肪酸 (FFA) 可通过多种途径诱导炎症反应。铁死亡的特征是由铁积累导致的脂质过氧化产物积累和致命的反应性氧物质, 这可能是炎性损伤的上游事件。目的:研究 FFA诱导的病理毛细胞炎症损伤过程中铁死亡的参与及其机制。材料和方法:我们利用 House Ear Institute-Organ of Corti 1 (HEI-OC1) 细胞系作为体外模型。 棕榈酸 (PA) 被用作 FF...


  • Open Access

    The Comorbidity of Depression and Anxiety Symptoms in Tinnitus Sufferers: A Network Analysis

    by Xuemin Chen, Lei Ren, Xinmiao Xue, Ning Yu, Peng Liu, Weidong Shen, Hanwen Zhou, Ben Wang, Jingcheng Zhou, Shiming Yang, et al.

    Objective: Sufferers of tinnitus, especially of the prolonged type, frequently suffer from comorbid depression and anxiety. From the perspective of the network model, this comorbidity is thought to be an interacting system of these two symptoms. In our study, we conducted a network analysis of depression and anxiety comorbidity in tinnitus sufferers, aiming to identify the central and bridge symptoms and make informed suggestions for clinical interventions and psychotherapy. Method: A total of 566 tinnitus sufferers were enrolled in our study. The Patient Health Questionnaire-9 (PHQ-9) and the Generalized Anxiety Disorder 7-Item Questionnaire (GAD-7) were selected to evaluate depression and anxiety symptoms, respectively, followed by network analysis to construct the interacting networks. Results: The findings identified six edges of strongest regularized partial correlations in this network. Of these, three were depression symptoms and three were anxiety symptoms. The anxiety symptoms “Unable to control worry” and “Relaxation difficulty” and the depression symptom “Feeling depressed or hopeless” had the highest expected influence centrality. The analysis results also revealed three bridge symptoms: “Afraid something awful might happen”, “Feeling of worthlessness”, and “Trouble concentrating”. As for “Suicidal ideation”, the direct relations between this symptom and “Afraid something awful might happen” and “Feeling depressed or hopeless” were the strongest. Conclusions: The central and bridge symptoms of the interacting network of depression and anxiety symptoms in tinnitus sufferers can be considered a significant transdiagnostic intervention target for the management of this comorbidity. In particular, clinical prevention and psychotherapy should be implemented, targeting the symptoms that have the strongest associations with suicidal ideation.


  • Open Access

    NT5E upregulation in head and neck squamous cell carcinoma: A novel biomarker on cancer-associated fibroblasts for predicting immunosuppressive tumor microenvironment

    by Xue-Min Chen, Yu-Yang Liu, Bing-Yan Tao, Xin-Miao Xue, Xin-Xin Zhang, Lin-Lin Wang, Hui Zhong, Jun Zhang, Shi-Ming Yang, Qing-Qing Jiang

    Despite tremendous progress made in the diagnosis and managements, head and neck squamous cell carcinoma (HNSC) remains a global medical dilemma with dismal clinical prognosis and high mortality. Gene NT5E encodes the ecto-5’-nucleotidase (CD73), which facilitates the formation of immunosuppressive tumor microenvironment (TME) permissive for tumor progression in various malignancies. Nevertheless, the cell subsets NT5E expressed on and the potential function of NT5E in the TME of HNSC remain virgin lands in HNSC. In this study, we comprehensively performed integrated prognostic analysis and elucidated that NT5E was an independent prognostic indicator for HNSC, for which a high NT5E level predicted poor overall survival (OS), disease-specific survival (DSS) and progression-free interval (PFI) in HNSC patients (ppppIn-situ multicolor immunofluorescence staining was later conducted and the results further verified our findings. Taken together, NT5E could be a novel biomarker in HNSC. Predominantly expressed on CAFs, the upregulation of NT5E might predict an immunosuppressive TME for HNSC patients who may benefit little from immunotherapy. Targeting CAFs with high NT5E expression might be a novel therapeutic strategy for HNSC patients.


  • Open Access

    The Role of Genetic Variants in the Susceptibility of Noise-Induced Hearing Loss

    by Xue-Min Chen, Xin-Miao Xue, Ning Yu, Wei-Wei Guo, Shuo-Long Yuan, Qing-Qing Jiang, Shi-Ming Yang

    Noised-induced hearing loss (NIHL) is an acquired, progressive neurological damage caused by exposure to intense noise in various environments including industrial, military and entertaining settings. The prevalence of NIHL is much higher than other occupational injuries in industrialized countries. Recent studies have revealed that genetic factors, together with environmental conditions, also contribute to NIHL. A group of genes which are linked to the susceptibility of NIHL had been uncovered, involving the progression of oxidative stress, potassium ion cycling, cilia structure, heat shock protein 70 (HSP70), DNA damage repair, apoptosis, and some other genes. In this review, we briefly summarized the studies primary in population and some animal researches concerning the susceptible genes of NIHL, intending to give insights into the further exploration of NIHL prevention and individual treatment.


  • Microstate in resting state: an EEG indicator of tinnitus?

    by Wei Cao, Fangyuan Wang, Chi Zhang, Guangxiong Lei, Qingqing Jiang, Weidong Shen, Shiming Yang

    Background: Tinnitus was a subjective auditory phantom phenomenon which could be highly distressing and had no objective indicators for evaluation. Objectives: The aim of this study was to investigate whether and how did electroencephalography (EEG) microstates of subjective tinnitus patients change in resting state and whether could be an objective indicator for tinnitus. Material and Methods: We enrolled chronic subjective tinnitus patients and matched age and gender with healthy controls. EEG recording, microstate analysis and statistical analysis were performed. Results: We finally had 10 male and 8 female age-matched participants in tinnitus group and healthy control group. Statistical differences were found in the microstate A, C and D durations between the two groups (class A, p = .024; class B, p = .018; class D, p = .029). Microstate durations of class A and D had linear correlation with VAS scores in tinnitus patients (microstate A [R spare = 0.43, p = .003*]; microstate D [R spare = 0.46, p = .002*]). Conclusions: Microstates had changed in chronic tinnitus patients and provided an indicator or perspective to explore the mechanisms of tinnitus. The maintenance of chronic subjective tinnitus may be related to changes in cerebral cortex activity.


  • Open Access

    Degeneration of saccular hair cells caused by MITF gene mutation

    by Yi Du, Li-Li Ren, Qing-Qing Jiang, Xing-Jian Liu, Fei Ji, Yue Zhang, Shuo-Long Yuan, Zi-Ming Wu, Wei-Wei Guo, Shi-Ming Yang

    Background: Waardenburg syndrome (WS) is the consequence of an inherited autosomal dominant mutation which causes the early degeneration of intermediate cells of cochlear stria vascularis (SV) and profound hearing loss. Patients with WS may also experience primary vestibular symptoms. Most of the current WS studies did not discuss the relationship between WS and abnormal vestibular function. Our study found that a spontaneous mutant pig showed profound hearing loss and depigmentation. MITF-M, a common gene mutation causes type WS which affect the development of the intermediate cell of SV, was then identified for animal modeling. Results: In this study, the degeneration of vestibular hair cells was found in pigs with MITF-M. The morphology of hair cells in vestibular organs of pigs was examined using electron microscopy from embryonic day E70 to postnatal two weeks. Significant hair cell loss in the mutant saccule was found in this study through E95 to P14. Conversely, there was no hair cell loss in either utricle or semi-circular canals. Conclusions: Our study suggested that MITF-M gene mutation only affects hair cells of the saccule, but has no effect on other vestibular organs. The study also indicated that the survival of cochlear and saccular hair cells was dependent on the potassium release from the cochlear SV, but hair cells of the utricle and semi-circular canals were independent on SV.