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Gastric cancer (GC) remains a predominant form of malignant tumor globally, necessitating innovative non-surgical therapeutic approaches. This investigation aimed to delineate the expression landscape of macrophage-associated genes in GC and to evaluate their prognostic significance and influence on immunotherapeutic responsiveness. Utilizing the CellMarker2.0 database, we identified 69 immune cell markers with prognostic relevance in GC, including 12 macrophage-specific genes. A Weighted Gene Co-Expression Network Analysis (WGCNA) isolated 3,181 genes correlated with these macrophage markers. The Cancer Genome Atlas (TCGA-STAD) dataset was employed as the training set, while data from the GSE62254 served as the validation cohort. 13 genes were shortlisted through LASSO-Cox regression to formulate a prognostic model. Multivariable Cox regression substantiated that the calculated risk score serves as an imperative independent predictor of overall survival (OS). Distinct macrophage infiltration profiles, pathway associations, treatment susceptibilities, and drug sensitivities were observed between high- and low-risk groups. The preliminary validation of ANXA5 in predicting the survival rates of GC patients at 1 year, 3 years, and 5 years, as well as its expression levels were higher and role in promoting tumor angiogenesis in GC through immunohistochemistry and angiogenesis experiments. In summary, macrophage-related genes were potentially a novel crosstalk mechanism between macrophages and endothelial cells in the tumor microenvironment, and the interplay between inflammation and angiogenesis might have also offered new therapeutic targets, providing a new avenue for personalized treatment interventions.
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Neoplasias Gástricas , Humanos , Pronóstico , Neoplasias Gástricas/genética , Neoplasias Gástricas/terapia , Angiogénesis , Células Endoteliales , Inmunoterapia , Anexina A5 , Microambiente Tumoral/genéticaRESUMEN
OBJECTIVE: This study aimed to explore the clinical relevance of heat shock protein family A member 6 (HSPA6) in gastric cancer (GC) and its effect on GC cell proliferation. METHODS: HSPA6 mRNA and protein levels were analyzed by bioinformatics, RT-qPCR, western blot and immunohistochemistry. HSPA6 was correlated with clinicopathological variables by the Chi-square test. Kaplan-Meier survival analysis and the univariate and multivariate Cox models were used to assess the prognostic value of HSPA6. Nomogram was used to predict overall survival in patients with GC. Knockdown or over-expression of HSPA6 in GC cell lines was constructed by lentiviral transduction. EdU and CCK-8 assay were used to detect cell proliferation. In vivo mouse tumor models were performed to evaluate the effects of HSPA6 on GC growth. RESULTS: HSPA6 were significantly upregulated in the GC tissues compared to the normal stomach epithelium and were associated with Ming classification (p < 0.001) and tumor size (p = 0.002). Patients with high expression of HSPA6 showed worse survival compared to the low expression group. HSPA6 was identified to be an independent prognostic biomarker for GC. HSPA6 was functionally annotated with the cell cycle, G2M checkpoint and Hippo pathway. Knockdown of HSPA6 suppressed XGC-1 cell proliferation both in vitro and in vivo. Overexpression of HSPA6 in AGS cells increased proliferation rates, increased the levels of cyclinB1 and YAP and decreased that of phosphorylated YAP. HSPA6 knockdown in the NUGC2 cells had the opposite effect. CONCLUSIONS: HSPA6 promotes GC proliferation by the Hippo pathway, as a novel prognostic biomarker and potential therapeutic target.
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Neoplasias Gástricas , Animales , Ratones , Pronóstico , Neoplasias Gástricas/patología , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Estimación de Kaplan-Meier , Proliferación Celular/genética , Línea Celular Tumoral , Regulación Neoplásica de la Expresión GénicaRESUMEN
Gastric cancer (GC) is a malignant tumor that originates from the epithelium of the gastric mucosa. The latest global cancer statistics show that GC ranks fifth in incidence and fourth in mortality among all cancers, posing a serious threat to public health. While early-stage GC is primarily treated through surgery, chemotherapy is the frontline option for advanced cases. Currently, commonly used chemotherapy regimens include FOLFOX (oxaliplatin + leucovorin + 5-fluorouracil) and XELOX (oxaliplatin + capecitabine). However, with the widespread use of chemotherapy, an increasing number of cases of drug resistance have emerged. This article primarily explores the potential mechanisms of chemotherapy resistance in GC patients from five perspectives: cell death, tumor microenvironment, non-coding RNA, epigenetics, and epithelial-mesenchymal transition. Additionally, it proposes feasibility strategies to overcome drug resistance from four angles: cancer stem cells, tumor microenvironment, natural products, and combined therapy. The hope is that this article will provide guidance for researchers in the field and bring hope to more GC patients.
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Neoplasias Gástricas , Humanos , Neoplasias Gástricas/tratamiento farmacológico , Neoplasias Gástricas/genética , Oxaliplatino/uso terapéutico , Desoxicitidina , Capecitabina/uso terapéutico , Fluorouracilo/uso terapéutico , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Leucovorina/uso terapéutico , Resistencia a Medicamentos , Microambiente TumoralRESUMEN
Colorectal cancer (CRC) is one of the most common gastrointestinal malignancies in the world. With the rapid pace of life and changes in diet structure, the incidence and mortality of CRC increase year by year posing a serious threat to human health. As the most complex and largest microecosystem in the human body, intestinal microecology is closely related to CRC. It is an important factor that affects and participates in the occurrence and development of CRC. Advances in next-generation sequencing technology and metagenomics have provided new insights into the ecology of gut microbes. It also helps to link intestinal flora with CRC, and the relationship between intestinal flora and CRC can be continuously understood from different levels. This paper summarizes the relationship between intestinal flora and CRC and its potential role in the diagnosis of CRC providing evidence for early screening and treatment of CRC.
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BACKGROUND: Colorectal cancer has a high incidence and mortality rate due to a low rate of early diagnosis. Therefore, efficient diagnostic methods are urgently needed. PURPOSE: This study assesses the diagnostic effectiveness of Carbohydrate Antigen 19-9 (CA19-9), Carcinoembryonic Antigen (CEA), Alpha-fetoprotein (AFP), and Cancer Antigen 125 (CA125) serum tumor markers for colorectal cancer (CRC) and investigates a machine learning-based diagnostic model incorporating these markers with blood biochemical indices for improved CRC detection. METHOD: Between January 2019 and December 2021, data from 800 CRC patients and 697 controls were collected; 52 patients and 63 controls attending the same hospital in 2022 were collected as an external validation set. Markers' effectiveness was analyzed individually and collectively, using metrics like ROC curve AUC and F1 score. Variables chosen through backward regression, including demographics and blood tests, were tested on six machine learning models using these metrics. RESULT: In the case group, the levels of CEA, CA199, and CA125 were found to be higher than those in the control group. Combining these with a fourth serum marker significantly improved predictive efficacy over using any single marker alone, achieving an Area Under the Curve (AUC) value of 0.801. Using stepwise regression (backward), 17 variables were meticulously selected for evaluation in six machine learning models. Among these models, the Gradient Boosting Machine (GBM) emerged as the top performer in the training set, test set, and external validation set, boasting an AUC value of over 0.9, indicating its superior predictive power. CONCLUSION: Machine learning models integrating tumor markers and blood indices offer superior CRC diagnostic accuracy, potentially enhancing clinical practice.
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Lysosomal-dependent cell death (LDCD) has an excellent therapeutic effect on apoptosis-resistant and drug-resistant tumors; however, the important role of LDCD-related genes (LDCD-RGs) in kidney renal clear cell carcinoma (KIRC) has not been reported. Initially, single-cell atlas of LDCD signal in KIRC was comprehensively depicted. We also emphasized the molecular characteristics of LDCD-RGs in various human neoplasms. Predicated upon the expressive quotients of LDCD-RGs, we stratified KIRC patients into tripartite cohorts denoted as C1, C2, and C3. Those allocated to the ambit of C1 evinced the most sanguine prognosis within the KIRC cohort, underscored by the acme of LDCD-RGs scores. This further confirms the significant role that LDCD-RGs play in both the pathophysiological foundation and clinical implications of KIRC. In culmination, by virtue of employing the LASSO-Cox analytical modality, we have ushered in an innovative and avant-garde prognostic framework tailored for KIRC, predicated on the bedrock of LDCD-RGs. The assemblage of KIRC instances was arbitrarily apportioned into constituents inclusive of a didactic cohort, an internally wielded validation cadre, and an externally administered validation cohort. Concurrently, patients were dichotomized into strata connoting elevated jeopardy synonymous with adverse prognostic trajectories, and conversely, diminished risk tantamount to favorable prognoses, contingent on the calibrated expressions of LDCD-RGs. Succinctly, our investigative findings serve to underscore the cardinal capacity harbored by LDCD-RGs within the KIRC milieu, concurrently birthing a pioneering prognostic schema intrinsically linked to the trajectory of KIRC and its attendant prognoses.
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Carcinoma de Células Renales , Neoplasias Renales , Humanos , Pronóstico , Carcinoma de Células Renales/genética , Muerte Celular , Neoplasias Renales/genética , RiñónRESUMEN
Recently, various cancer types have been identified to express a distinct subset of Interferon-stimulated genes (ISGs) that mediate therapy resistance. The mechanism through which cancer cells maintain prolonged Interferon stimulation effects to coordinate resistance remains unclear. Our research demonstrated that aberrant upregulation of TAGLN2 is associated with gastric cancer progression, and inhibiting its expression renders gastric cancer cells more susceptible to chemotherapy and radiation. We uncovered a novel role for TAGLN2 in the upregulation of resistance signature ISGs by enhancing YBX1-associated ssDNA aggregation and cGAS-STING pathway activation. TAGLN2 modulates YBX1 by recruiting c-Myc and SOX9 to YBX1 promoter region and directly interacting with AKT-YBX1, thereby enhancing YBX1 phosphorylation and nuclear translocation. Significantly, targeted downregulation of key proteins, inhibition of the TAGLN2-YBX1-AKT interaction (using Fisetin or MK2206) or disruption of the cGAS-STING pathway substantially reduced ssDNA accumulation, subsequent ISGs upregulation, and therapy resistance. The combination of Cisplatin with MK2206 displayed a synergistic effect in the higher TAGLN2-expressing xenograft tumors. Clinical analysis indicated that a derived nine-gene set effectively predicts therapeutic sensitivity and long-term prognosis in gastric cancer patients. These findings suggest that TAGLN2, YBX1 and induced ISGs are novel predictive markers for clinical outcomes, and targeting this axis is an attractive therapeutic sensitization strategy.
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Daño del ADN , Proteínas Proto-Oncogénicas c-akt , Transducción de Señal , Neoplasias Gástricas , Proteína 1 de Unión a la Caja Y , Humanos , Neoplasias Gástricas/genética , Neoplasias Gástricas/patología , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/tratamiento farmacológico , Proteína 1 de Unión a la Caja Y/metabolismo , Proteína 1 de Unión a la Caja Y/genética , Proteínas Proto-Oncogénicas c-akt/metabolismo , Animales , Línea Celular Tumoral , Ratones , Resistencia a Antineoplásicos/genética , Compuestos Heterocíclicos con 3 Anillos/farmacología , Ratones Desnudos , Interferones/metabolismo , Regulación Neoplásica de la Expresión Génica , Cisplatino/farmacología , Cisplatino/uso terapéutico , Proteínas de Microfilamentos/metabolismo , Proteínas de Microfilamentos/genética , Nucleotidiltransferasas/metabolismo , Nucleotidiltransferasas/genética , Femenino , Proteínas de la Membrana/metabolismo , Proteínas de la Membrana/genética , Ratones Endogámicos BALB C , MasculinoRESUMEN
Background: Osteoporosis is becoming more common worldwide, imposing a substantial burden on individuals and society. The onset of osteoporosis is subtle, early detection is challenging, and population-wide screening is infeasible. Thus, there is a need to develop a method to identify those at high risk for osteoporosis. Objective: This study aimed to develop a machine learning algorithm to effectively identify people with low bone density, using readily available demographic and blood biochemical data. Methods: Using NHANES 2017-2020 data, participants over 50 years old with complete femoral neck BMD data were selected. This cohort was randomly divided into training (70%) and test (30%) sets. Lasso regression selected variables for inclusion in six machine learning models built on the training data: logistic regression (LR), support vector machine (SVM), gradient boosting machine (GBM), naive Bayes (NB), artificial neural network (ANN) and random forest (RF). NHANES data from the 2013-2014 cycle was used as an external validation set input into the models to verify their generalizability. Model discrimination was assessed via AUC, accuracy, sensitivity, specificity, precision and F1 score. Calibration curves evaluated goodness-of-fit. Decision curves determined clinical utility. The SHAP framework analyzed variable importance. Results: A total of 3,545 participants were included in the internal validation set of this study, of whom 1870 had normal bone density and 1,675 had low bone density Lasso regression selected 19 variables. In the test set, AUC was 0.785 (LR), 0.780 (SVM), 0.775 (GBM), 0.729 (NB), 0.771 (ANN), and 0.768 (RF). The LR model has the best discrimination and a better calibration curve fit, the best clinical net benefit for the decision curve, and it also reflects good predictive power in the external validation dataset The top variables in the LR model were: age, BMI, gender, creatine phosphokinase, total cholesterol and alkaline phosphatase. Conclusion: The machine learning model demonstrated effective classification of low BMD using blood biomarkers. This could aid clinical decision making for osteoporosis prevention and management.
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Densidad Ósea , Aprendizaje Automático , Osteoporosis , Humanos , Femenino , Persona de Mediana Edad , Masculino , Osteoporosis/diagnóstico , Anciano , Algoritmos , Encuestas Nutricionales , Modelos Logísticos , Máquina de Vectores de SoporteRESUMEN
Patients with infiltrative-type gastric cancer (GC) (Ming's classification) have a poor prognosis due to more metastasis and recurrence. Cancer-associated fibroblasts (CAFs) in infiltrative-type extracellular matrix (ECM) have specific characteristics compared with those of expansive types with respect to metastasis, but the mechanism is still unclear. Based on our proteomics data, TCGA data analysis, and immunohistochemical staining results, significantly higher expression of IGFBP7 was observed in GC, especially in the infiltrative type, and was associated with a poor prognosis. Combining single-cell transcriptome data from GEO and multiple immunofluorescence staining on tissue showed that the differential expression of IGFBP7 mainly originated from myofibroblastic CAFs, the subgroup with higher expression of PDGFRB and α-SMA. After treating primary normal fibroblasts (NFs) with conditional medium or recombined protein, it was demonstrated that XGC-1-derived TGF-ß1 upregulated the expression of IGFBP7 in the cells and its secretion via the P-Smad2/3 pathway and mediated its activation with higher FAP, PDGFRB, and α-SMA expression. Then, either conditional medium from CAFs with IGFBP7 overexpression or recombined IGFBP7 protein promoted the migration, invasion, colony formation, and sphere growth ability of XGC-1 and MGC-803, respectively. Moreover, IGFBP7 induced EMT in XGC-1. Therefore, our study clarified that in the tumor microenvironment, tumor-cell-derived TGF-ß1 induces the appearance of the IGFBP7+ CAF subgroup, and its higher IGFBP7 extracellular secretion level accelerates the progression of tumors.
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Tumor microenvironment and heterogeneity play vital roles in the development and progression of gastric cancer (GC). In the past decade, a considerable amount of single-cell RNA-sequencing (scRNA-seq) studies have been published in the fields of oncology and immunology, which improve our knowledge of the GC immune microenvironment. However, much uncertainty still exists about the relationship between the macroscopic and microscopic data in transcriptomics. In the current study, we made full use of scRNA-seq data from the Gene Expression Omnibus database (GSE134520) to identify 25 cell subsets, including 11 microenvironment-related cell types. The MIF signaling pathway network was obtained upon analysis of receptor-ligand pairs and cell-cell interactions. By comparing the gene expression in a wide variety of cells between intestinal metaplasia and early gastric cancer, we identified 64 differentially expressed genes annotated as immune response and cellular communication. Subsequently, we screened these genes for prognostic clinical value based on the patients' follow-up data from The Cancer Genome Atlas. TMPRSS15, VIM, APOA1, and RNASE1 were then selected for the construction of LASSO risk scores, and a nomogram model incorporating another five clinical risk factors was successfully created. The effectiveness of least absolute shrinkage and selection operator risk scores was validated using gene set enrichment analysis and levels of immune cell infiltration. These findings will drive the development of prognostic evaluations affected by the immune tumor microenvironment in GC.
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GC is a fatal disease with high heterogeneity and invasiveness. Recently, SPP1 has been reported to be involved in the tumor progression of multiple human cancers; however, the role of SPP1 in GC heterogeneity and whether it is associated with the invasiveness and mortality of GC remain unclear. Here, we combined multiple RNA sequencing approaches to evaluate the impact of SPP1 on GC. Through bulk RNA sequencing (bulk RNA-seq) and immunohistochemistry (IHC), we found that SPP1 was highly expressed in GC, and high levels of SPP1 were associated with macrophage infiltration, an advanced tumor stage, and higher mortality for advanced GC patients. Furthermore, through simultaneous single-cell and spatial analysis, we demonstrated that SPP1+ macrophages are tumor-specific macrophages unique to cancer and enriched in the deep layer of GC tissue. Cell-cell communication analysis revealed that SPP1/CD44 interactions between SPP1+ macrophages and their localized tumor epithelial cells could activate downstream target genes in epithelial cells to promote dynamic changes in intratumor heterogeneity. Moreover, these activated genes were found to be closely associated with poor clinical GC outcomes and with cancer-related pathways that promote GC progression, as shown by survival analysis and enrichment analysis, respectively. Collectively, our study reveals that tumor-specific SPP1+ macrophages drive the architecture of intratumor heterogeneity to evolve with tumor progression and that SPP1 may serve as a prognostic marker for advanced GC patients, as well as a potential therapeutic target for GC.
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Gastric Cancer (GC) is one of the main causes leading to death. PMP22, as a member of the GAS3 family of tetraspan proteins, it is associated with a variety of neurological diseases. Recently, more and more studies have shown that PMP22 play a great role in the physiological processes such as cells adhesion, migration, proliferation and tumorigenesis, but the involvement and functional mechanisms of PMP22 in Gastric carcinoma are not investigated clearly. In this study, we found that the PMP22 was overexpressed in the GC cells and tissue. Knockdown of PMP22 inhibits cell growth. Over-expressed PMP22 inhibits the etoposide-induced apoptosis, meanwhile knockdown of PMP22 promotes the etoposide-induced proliferation suppression, and increases cell apoptosis in GC cells. Furthermore, PMP22 enhanced the inhibition of the p53 transcriptional activities and down-regulated the p53 targeting genes, including p21, BAX and PUMA with or without treatment of etoposide. Finally, our results showed that PMP22 reduced the etoposide-induced tumor growth suppression in nude mice. Taken together, our research provided an anti-apoptotic properties alternative mechanism for PMP22 in gastric carcinoma and suggested PMP22 can be a potential target for the treatment of gastric cancer.
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Antineoplásicos Fitogénicos/farmacología , Apoptosis/efectos de los fármacos , Etopósido/farmacología , Proteínas de la Mielina/antagonistas & inhibidores , Neoplasias Gástricas/tratamiento farmacológico , Proteína p53 Supresora de Tumor/metabolismo , Animales , Western Blotting , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Femenino , Citometría de Flujo , Regulación Neoplásica de la Expresión Génica/fisiología , Humanos , Lentivirus/genética , Masculino , Ratones , Persona de Mediana Edad , Proteínas de la Mielina/genética , Plásmidos , Interferencia de ARN , Reacción en Cadena en Tiempo Real de la Polimerasa , Transducción de Señal , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patología , Transfección , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
CONCLUSIONS: Pharyngeal constrictor muscle injury and fatty changes may play important roles in the pathogenesis and progression of OSAHS. OBJECTIVE: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a respiratory disorder caused by upper airway obstruction during sleep. The primary objectives of this study were to determine the ultrastructural characteristics of the pharyngeal constrictor muscle in patients with OSAHS. METHODS: A pharyngeal constrictor muscle specimen was collected from all subjects. The muscle cell ultrastructure was observed under electron microscopy. RESULTS: Eighteen male patients with OSAHS (OSAHS group) and 10 male body mass index-matched patients with chronic tonsillitis (control group) were enrolled in this study. All patients were obese adults. The apnea-hypopnea index (41.22 ± 17.29 vs 2.30 ± 1.10 events/h) was significantly higher and the lowest arterial oxygen saturation (76.00 ± 8.57% vs 97.00 ± 2.00%) was significantly lower in the OSAHS group than in the control group (both p < 0.001). Myofibril disorder, mitochondrial edema, and intramyocellular lipid droplets were observed in patients with OSAHS. There was a significant correlation between the number of lipid droplets and the apnea-hypopnea index.
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Gotas Lipídicas/ultraestructura , Músculos Faríngeos/ultraestructura , Apnea Obstructiva del Sueño/patología , Adulto , Estudios de Casos y Controles , Humanos , Masculino , Persona de Mediana Edad , Obesidad/complicaciones , Estudios Prospectivos , Apnea Obstructiva del Sueño/etiologíaRESUMEN
CONCLUSION: Noise exposure can cause a decline in cochlear ribbon synapses and result in consequent hearing loss. The reduction of synaptic puncta appears reversible and may contribute to hearing restoration in mice after noise exposure. OBJECTIVE: To detect whether noise induced reversible changes of cochlear ribbon synapses contribute to temporary hearing loss in C57BL/6J mice. METHODS: The mice were assigned randomly to five groups and exposed to white noise at 110 dB SPL for 2 h except the control group. ABR thresholds were acquired before noise exposure (control), immediately following exposure (Day 0), or on Days 4, 7, or 14 after noise exposure. Light microscopy, scanning emission microscopy, and whole mounts examination was utilized to study whether there is morphology change of outer hair cells (OHC), inner hair cells (IHC), or spiral ganglion cells (SGN) due to the 110 dB white noise. Moreover, experimental approaches, including immunostaining and confocal microcopy, were used to detect whether ribbon synapses were the primary targets of noise-induced temporary hearing loss. RESULT: Exposure to 110 dB white noise for 2 h induced TTS in mice, with the maximal ABR threshold elevations seen on the 4(th) day after noise exposure. There were no significant morphological changes in the cochlea. Paralleled changes of pre-synaptic ribbons in both the number and post-synaptic density (PSDs) during this noise exposure were detected. The number of pre-synaptic ribbon, post-synaptic density (PSDs), and co-localized puncta correlated with the shifts of ABR thresholds. Moreover, a complete recovery of ABR thresholds and synaptic puncta was seen on the 14(th) day after the noise stimulations.
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Umbral Auditivo/fisiología , Cóclea/fisiopatología , Potenciales Evocados Auditivos del Tronco Encefálico/fisiología , Células Ciliadas Auditivas Internas/ultraestructura , Células Ciliadas Auditivas Externas/ultraestructura , Pérdida Auditiva Provocada por Ruido/patología , Estimulación Acústica/efectos adversos , Animales , Cóclea/metabolismo , Cóclea/ultraestructura , Modelos Animales de Enfermedad , Células Ciliadas Auditivas Internas/metabolismo , Células Ciliadas Auditivas Externas/metabolismo , Pérdida Auditiva Provocada por Ruido/metabolismo , Pérdida Auditiva Provocada por Ruido/fisiopatología , Ratones , Ratones Endogámicos C57BL , Microscopía Confocal , Microscopía Electrónica de Rastreo , Plasticidad Neuronal , Ganglio Espiral de la Cóclea/metabolismo , Ganglio Espiral de la Cóclea/ultraestructura , SinapsisRESUMEN
OBJECTIVE: To investigate the effect of early phase debridement by the different intervention frequencies on postoperative symptoms recovery and turnover of mucosa after functional endoscopic sinus surgery (FESS). METHODS: 67 patients undergone FESS were divided into intervention group and control group. Intranasal corticosteroids, macrolides antibiotics and postoperative saline douching were used in both groups. Debridement was performed on the 1(st), 4(th), 8(th) postoperative week on patients of invention group, while once per week on patients of control group. The primary outcome measure was visual analogue scale (VAS) and Lund-Kennedy Endoscopic Score (LKES) Results: On the 4(th) week, the control group presented more release on nasal block, the VAS of the two groups is 3.45 ± 1.16 and 4.83 ± 1.47 in the control group and intervention group respectively which was significantly different. The LKES on crust decreased more in the control group (1.12 ± 0.64 in the control group and 1.90 ± 0.47 in the intervention group). However, the control group complained more sever facial pain and uncomfortable; the VAS of two groups is 5.92 ± 0.91 and 2.74 ± 1.41 respectively. On the 8(th) week, there were no significant difference between the two groups on all domains of VAS and LKES except lower scar was shown in the control group. CONCLUSIONS: Benefit of frequent debridement during the early postoperative was not in positive correlation with patients recovering from ESS. Excessive debridement may induce more surgical trauma and cause more facial pain to patients. Therefore, in terms of subjective recovery and health care costs, appropriate extending postoperative management time and decreasing intervention frequencies will not affect the therapeutic effect of endoscopic surgery for chronic sinusitis.
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Recent studies have reported that noise exposure at relatively low intensities can cause temporary threshold shifts (TTS) in hearing. However, the mechanism underlying the TTS is still on debate. Here, we report that an acoustic stimulation (100 dB SPL, white noise) induced TTS in mice, with the maximal ABR threshold elevations seen on the 4(th) day after noise exposure. On the other hand, there were no significant morphological changes in the cochlea. Further, there were paralleled changes of pre-synaptic ribbons in both the number and postsynaptic density (PSDs) during this noise exposure. The numbers of presynaptic ribbon, postsynaptic density (PSDs), and colocalized puncta correlated with the shifts of ABR thresholds. Moreover, a complete recovery of ABR thresholds and synaptic puncta was seen on the 14(th) day after the noise stimulations. Thus, our study may indicate that noise exposure can cause a decline in cochlear ribbon synapses and result in consequent hearing loss. The reduction of synaptic puncta appears reversible and may contribute to hearing restoration in mice after noise exposure.