ObjectiveTo analyze the epidemiological trends and characteristics of brucellosis in humans (hereinafter referred to as brucellosis) in Tangshan City, Hebei Province from 2016 to 2023, and to provide a scientific basis for formulating brucellosis prevention and control strategies in the region. MethodsThe incidence data of human brucellosis in Tangshan City from 2016 to 2023 were collected from the China Disease Prevention and Control Information System. The diagnosis time, infection route, and clinical characteristics of the cases were obtained from the case investigation reports. Descriptive epidemiological methods were used to analyze the temporal, spatial, demographic distributions, and clinical characteristics of human brucellosis. Brucella species were identified using agglutination tests with bacterial suspension and A/M antigen-positive serum. ResultsA total of 2 193 cases of human brucellosis were confirmed and clinically diagnosed in Tangshan City from 2016 to 2023, with the peak incidence occured from March to August, and which exhibited distinct geographic distribution patterns. The highest incidence rate was found in people aged 60‒<70 years. The occupation of cases were primarily farmers. The incidence rate in males (528/100 000) was higher than that in females (184/100 000). All cases had confirmed exposure to infected animals or contaminated animal products. ConclusionThe epidemic of human brucellosis in Tangshan exhibited an overall steady downward trend from 2016 to 2023, except for a slight increase in 2016 and 2021, with the incidence rate controlled at 289/100 000‒335/100 000. The prevention and control situation of human brucellosis still remains severe, with the highest incidence rate in the eastern region of Tangshan, which are characterized by the breeding, slaughtering, and processing of cattle and sheep. Therefore, it it is necessary to enhance the prevention and control of human brucellosis among the personnel engaged in these industries in the eastern areas.

Hearing loss is the most prevalent disabling disease. Cochlear implantation（CI） serves as the primary intervention for severe to profound hearing loss. This consensus systematically explores the value of genetic diagnosis in the pre-operative assessment and efficacy prognosis for CI. Drawing upon domestic and international research and clinical experience, it proposes an evidence-based medicine three-tiered prognostic classification system（Favorable, Marginal, Poor）. The consensus focuses on common hereditary non-syndromic hearing loss（such as that caused by mutations in genes like GJB2, SLC26A4, OTOF, LOXHD1） and syndromic hereditary hearing loss（such as Jervell & Lange-Nielsen syndrome and Waardenburg syndrome）, which are closely associated with congenital hearing loss, analyzing the impact of their pathological mechanisms on CI outcomes. The consensus provides recommendations based on multiple round of expert discussion and voting. It emphasizes that genetic diagnosis can optimize patient selection, predict prognosis, guide post-operative rehabilitation, offer stratified management strategies for patients with different genotypes, and advance the application of precision medicine in the field of CI.
Humans ; Cochlear Implantation ; Prognosis ; Hearing Loss/surgery* ; Consensus ; Connexin 26 ; Mutation ; Sulfate Transporters ; Connexins/genetics*

OBJECTIVES: To investigate the impact of high expression of transmembrane and coiled helix structural domain 1 (TMCO1) on prognosis of gastric cancer and the possible mechanisms. METHODS: TMCO1 expression in gastric cancer and its effect on gastric cancer progression and prognosis were analyzed using publicly available databases and clinical data of patients undergoing radical surgery in our hospital, and its possible biological functions were explored using KEGG and GO analyses. In gastric cancer HGC-27 cells, the effects of lentivirus-mediated TMCO1 overexpression and TMCO1 silencing on cell apoptosis, proliferation, invasion and migration were examined. RESULTS: TMCO1 expression was significantly elevated in gastric cancer tissues (P<0.05), and its high expression was positively correlated with cancer progression (P<0.001) and a lowered postoperative 5-year survival rate of the patients (P<0.05). Bioinformatic analyses suggested that TMCO1 may affect gastric cancer cell apoptosis via Wnt signaling. In HGC-27 cells, TMCO1 overexpression significantly promoted tumor cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion, whereas TMCO1 silencing produced the opposite effects. Western blotting showed that β-catenin levels were significantly upregulated in TMCO1-overexpressing cells and downregulated in cells with TMCO1 silencing. CONCLUSIONS TMCO1 is overexpressed in gastric cancer tissues, and its high expression promotes gastric cancer progression and affects long-term prognosis of the patients possibly by activating the Wnt/ β-catenin signaling pathway to inhibit apoptosis of gastric cancer cells.
Humans ; Stomach Neoplasms/metabolism* ; Apoptosis ; Prognosis ; Cell Line, Tumor ; Cell Proliferation ; Cell Movement ; Wnt Signaling Pathway ; beta Catenin/metabolism* ; Gene Expression Regulation, Neoplastic

The ability to localize sound sources rapidly allows human beings to efficiently understand the surrounding environment. Previous studies have suggested that there is an auditory "where" pathway in the cortex for processing sound locations. The neural activation in regions along this pathway encodes sound locations by opponent hemifield coding, in which each unilateral region is activated by sounds coming from the contralateral hemifield. However, it is still unclear how these regions interact with each other to form a unified representation of the auditory space. In the present study, we investigated whether functional connectivity in the auditory "where" pathway encoded sound locations during passive listening. Participants underwent functional magnetic resonance imaging while passively listening to sounds from five distinct horizontal locations (-90°, -45°, 0°, 45°, 90°). We were able to decode sound locations from the functional connectivity patterns of the "where" pathway. Furthermore, we found that such neural representation of sound locations was primarily based on the coding of sound lateralization angles to the frontal midline. In addition, whole-brain analysis indicated that functional connectivity between occipital regions and the primary auditory cortex also encoded sound locations by lateralization angles. Overall, our results reveal a lateralization-angle-based representation of sound locations encoded by functional connectivity patterns, which could add on the activation-based opponent hemifield coding to provide a more precise representation of the auditory space.
Humans ; Sound Localization/physiology* ; Male ; Female ; Magnetic Resonance Imaging ; Young Adult ; Functional Laterality/physiology* ; Adult ; Brain Mapping ; Auditory Cortex/physiology* ; Acoustic Stimulation ; Auditory Pathways/physiology* ; Brain/physiology*

Sensorineural hearing loss (SNHL), the most commonly-occurring form of hearing loss, is caused mainly by injury to or the loss of hair cells and spiral ganglion neurons in the cochlea. Numerous environmental and physiological factors have been shown to cause acquired SNHL, such as ototoxic drugs, noise exposure, aging, infections, and diseases. Several programmed cell death (PCD) pathways have been reported to be involved in SNHL, especially some novel PCD pathways that have only recently been reported, such as ferroptosis, necroptosis, and pyroptosis. Here we summarize these PCD pathways and their roles and mechanisms in SNHL, aiming to provide new insights and potential therapeutic strategies for SNHL by targeting these PCD pathways.
Humans ; Hearing Loss, Sensorineural/metabolism* ; Necroptosis/drug effects* ; Pyroptosis/drug effects* ; Ferroptosis/drug effects* ; Animals

Objective: To investigate the effects of RING 1 and YY1 binding protein (RYBP), a member of the polycomb group (PcG), on bladder cancer cell proliferation and invasion, as well as the underlying mechanisms involved, so as to provide reference for the prevention and treatment of bladder cancer. Methods: Overexpressing and knocking down of RYBP were achieved in bladder cancer cell lines (T24, UM-UC-3, and 5637) via plasmids or siRNAs.Cell proliferation was assessed via thiazolyl blue (MTT) and colony formation assays, whereas migration was evaluated via scratch and Transwell assays.Changes in epithelial-mesenchymal transition (EMT) markers and other related proteins were examined with Western blotting. Results: RYBP overexpression significantly inhibited bladder cancer cell proliferation, invasion, and migration, whereas RYBP knockdown promoted these behaviors.Western blotting results revealed that RYBP overexpression downregulated the expressions of EMT markers N-cadherin, Vimentin, and Slug, but upregulated the expression of E-cadherin.Conversely, RYBP knockdown upregulated the expressions of N-cadherin, Vimentin, and Slug, while reducing the expression of E-cadherin. Conclusion: RYBP appears to inhibit the proliferation and migration of bladder cancer cells via the EMT pathway, indicating its potential application in bladder cancer therapies.

Objective:To explore the effect of staged pressure therapy, in addition to rehabilitation training, on scar hyperplasia and motor function after a deep hand burn.Methods:Sixty patients with deep hand burns were randomly divided into a control group ( n=30) and an observation group ( n=30). In addition to specialized burn treatment and early rehabilitation training, the control group was given routine pressure treatment, while the observation group was provided with staged pressure therapy for 6 months. Before the treatment and after 3 and 6 months of treatment, scar hyperplasia and hand function in both groups was evaluated using the Vancouver scar scale (VSS), grip strength and pinch strength tests, and the Jebsen hand function test (JHFT). Total active motion (TAM) and total passive motion (TPM) of the finger joints was quantified, and any complications during the treatment were recorded. Results:After 3 and 6 months of the treatment, all of the observations in both groups had improved significantly, but the improvements were significantly better among the treatment group, on average.Conclusions:Staged pressure therapy can more effectively inhibit scar hyperplasia after a deep hand burn. In conjunction with rehabilitation training, it better improves the mobility of the finger joints, hand muscle strength and the recovery of hand function. It is worthy of clinical promotion and application.

Objective:To explore any myogenic effect of extracorporeal shock wave therapy (ESWT) on shoulder joint contracture.Methods:Sixty-eight patients with shoulder contracture were enrolled and randomly divided into a conventional therapy group ( n=34) and an ESWT group ( n=34) for this clinical trial. The conventional therapy group received standard rehabilitation treatment, while the ESWT group received additional extracorporeal shock wave therapy. In addition, 24 Sprague-Dawley rats were randomly assigned to a blank control group, a model group, a natural recovery group, or an ESWT animal group, each of 6. All of the groups except the blank control group had contracture modeled using plaster cast immobilization of the left shoulder joint. After successful modeling, the natural recovery group was routinely raised for two weeks, while the ESWT animal group received two weeks of extracorporeal shock wave intervention. In both the clinical and animal experiments, ESWT was administered twice weekly (every Tuesday and Friday) for two consecutive weeks. Before and after the treatment, the patient groups were assessed using a visual analog scale (VAS) for pain, shoulder range of motion (ROM), and the root mean square (RMS) values of the surface electromyographs of the peri-shoulder muscles. Shoulder ROM was assessed in all four of the rat groups after the ESWT treatment, and histological analysis of the supraspinatus muscle was performed. Results:After the treatment, both patient groups showed significant improvements in their average VAS scores, active and passive shoulder ROM, and RMS values. On average, the ESWT group demonstrated significantly greater improvements than the conventional therapy group in active forward flexion, passive forward flexion, active abduction, passive abduction, and the RMS values of the deltoid, biceps brachii, and triceps brachii muscles. After the treatment the left shoulder abduction angle had been reduced significantly in the model group (to 96.00±2.37)°, the natural recovery group (103.00±4.05)° and the ESWT animal group (121.33±4.89)° compared to the blank control group (154.50±2.35)°. Both the natural recovery group and the ESWT animal group had significantly greater shoulder abduction angles than the model group, and the ESWT animal group also demonstrated a significantly larger abduction angle than the natural recovery group. After the treatment, significant differences between the model group and the blank control group were observed in the cross-sectional area of left supraspinatus muscle fibers and the proportion of collagen. The ESWT animal group too exhibited significantly improved muscle fiber cross-sectional area and collagen proportion compared to the natural recovery group.Conclusions:Shoulder joint contracture is accompanied by significant myopathic changes (muscle atrophy and fibrosis). ESWT effectively ameliorates these problems while enhancing muscle strength and functional recovery.

Objective To investigate the changes in eosinophil counts and the activation of microglial cells in the brain tissues of mice at different stages of Angiostrongylus cantonensis infection, and to examine the role of microglia in regulating the progression of angiostrongyliasis and unravel the possible molecular mechanisms. Methods Fifty BALB/c mice were randomly divided into the control group and the 7-d, 14-d, 21-day and 25-d infection groups, of 10 mice in each group. All mice in infection groups were infected with 30 stage III A. cantonensis larvae by gavage, and animals in the control group was given an equal amount of physiological saline. Five mice were collected from each of infection groups on days 7, 14, 21 d and 25 d post-infection, and 5 mice were collected from the control group on the day of oral gavage. The general and focal functional impairment was scored using the Clark scoring method to assess the degree of mouse neurological impairment. Five mice from each of infection groups were sacrificed on days 7, 14, 21 d and 25 d post-infection, and 5 mice from the control group were sacrificed on the day of oral gavage. Mouse brain tissues were sampled, and the pathological changes of brain tissues were dynamically observed using hematoxylin and eosin (HE) staining. Immunofluorescence staining with eosinophilic cationic protein (ECP) and ionized calcium binding adaptor molecule 1 (Iba1) was used to assess the degree of eosinophil infiltration and the counts of microglial cells in mouse brain tissues in each group, and the morphological parameters of microglial cells (skeleton analysis and fractal analysis) were quantified by using Image J software to determine the morphological changes of microglial cells. In addition, the expression of M1 microglia markers Fcγ receptor III (Fcgr3), Fcγ receptor IIb (Fcgr2b) and CD86 antigen (Cd86), M2 microglia markers Arginase 1 (Arg1), macrophage mannose receptor C-type 1 (Mrc1), chitinase-like 3 (Chil3), and phagocytosis genes myeloid cell triggering receptor expressed on myeloid cells 2 (Trem2), CD68 antigen (Cd68), and apolipoprotein E (Apoe) was quantified using real-time quantitative reverse transcription PCR (RT-qPCR) assay in the mouse cerebral cortex of mice post-infection. Results A large number of A. cantonensis larvae were seen on the mouse meninges surface post-infection, and many neuronal nuclei were crumpled and deeply stained, with a large number of bleeding points in the meninges. The median Clark scores of mouse general functional impairment were 0 (interquartile range, 0), 0 (interquartile range, 0.5), 6 (interquartile range, 1.0), 14 (interquartile range, 8.5) points and 20 (interquartile range, 9.0) points in the control group and the 7-d, 14-d, 21-d and 25-d groups, respectively (H = 22.45, P < 0.01), and the median Clark scores of mouse focal functional impairment were 0 (interquartile range, 0), 2 (interquartile range, 2.5), 7 (interquartile range, 3.0), 18 (interquartile range, 5.0) points and 25 (interquartile range, 6.5) points in the control group and the 7-d, 14-d, 21-d and 25-d groups, respectively (H = 22.72, P < 0.01). The mean scores of mice general and focal functional impairment were all higher in the infection groups than in the control group (all P values < 0.05). Immunofluorescence staining showed a significant difference in the eosinophil counts in mouse brain tissues among the five groups (F = 40.05, P < 0.000 1), and the eosinophil counts were significantly higher in mouse brain tissues in the 14-d (3.08 ± 0.78) and 21-d infection groups (5.97 ± 1.37) than in the control group (1.00 ± 0.28) (both P values < 0.05). Semi-quantitative analysis of microglia immunofluorescence showed a significant difference in the counts of microglial cells among the five groups (F = 17.66, P < 0.000 1), and higher Iba1 levels were detected in mouse brain tissues in 14-d (5.75 ± 1.28), 21-d (6.23 ± 1.89) and 25-d infection groups (3.70 ± 1.30) than in the control group (1.00 ± 0.30) (all P values < 0.05). Skeleton and fractal analyses showed that the branch length [(162.04 ± 34.10) μm vs. (395.37 ± 64.11) μm; t = 5.566, P < 0.05] and fractal dimension of microglial cells (1.30 ± 0.01 vs. 1.41 ± 0.03; t = 5.266, P < 0.05) were reduced in mouse brain tissues in the 21-d infection group relative to the control group. In addition, there were significant differences among the 5 groups in terms of M1 and M2 microglia markers Fcgr3 (F = 48.34, P < 0.05), Fcgr2b (F = 55.46, P < 0.05), Cd86 (F = 24.44, P < 0.05), Arg1 (F = 31.18, P < 0.05), Mrc1 (F = 15.42, P < 0.05) and Chil3 (F = 24.41, P < 0.05), as well as phagocytosis markers Trem2 (F = 21.19, P < 0.05), Cd68 (F = 43.95, P < 0.05) and Apoe (F = 7.12, P < 0.05) in mice brain tissues. Conclusions A. cantonensis infections may induce severe pathological injuries in mouse brain tissues that are characterized by massive eosinophil infiltration and persistent activation of microglia cells, thereby resulting in progressive deterioration of neurological functions.

Objective To investigate the feasibility of estimating the real-ear-to-coupler difference(RECD)in children with head circumference,so as to further optimize the personalized and accurate matching scheme of hearing aid fitting for children.Methods A total of 106 children(197 ears)were enrolled in this study.Head circumference was measured using a soft ruler and RECD was measured using OmetroricsAuricalTM.SPSS software was used to analyze the correlation between the head circumference,month age and RECD values at each frequency of children.Results ① The head circumference of boys was slightly larger than that of girls,but there was no significant differ-ence between them(P＞0.05).② Unitary linear correlation analysis showed that RECD values at 750-6 000 Hz were negatively correlated with the head circumference,and a regression equation was established between RECD values at 1 000-6 000 Hz and the head circumference.③ RECD values calculated by regression formula based on the head circumference showed no significant difference between 1 000-3 000 Hz and 6 000 Hz and children's actu-al RECD values.Conclusion The individual RECD values of 0-6 years old children were correlated with the head circumference,and with the increase of the head circumference,RECD values at middle and high frequencies de-creased gradually.For children whose physical developments were not consistent with biological age,the RECD data at middle and high frequencies could be estimated based on the head circumference.