ObjectiveTo observe the activation patterns and functional connectivity in the prefrontal cortex of patients with post-stroke anxiety (PSA) using functional near-infrared spectroscopy, in order to explore the underlying neural mechanism. MethodsFrom December, 2024 to September, 2025, 120 stroke patients were selected in Changzhou De'an Hospital. They were divided into PSA group (n = 60) and non-PSA group (n = 60) according to the score of Hamilton Anxiety Scale (HAMA). All patients wore an 18-channel fNIRS acquisition cap for detection. The differences in resting-state functional connectivity between the frontopolar cortex (FPC) and dorsolateral prefrontal cortex (DLPFC) were examined in both groups, as well as task-related activation in these brain regions. ResultsResting-state functional connectivity analysis revealed no statistically significant difference in network connectivity between two groups in the FPC and DLPFC regions (|t| < 1.301, P > 0.05). Task-related activation results revealed significantly reduced activation in the contralateral FPC of PSA group compared to the non-PSA group (Z = -2.063, P < 0.05). Activation levels in this region showed a negative correlation with the scores of HAMA (ρ = -0.201, P = 0.028). ConclusionActivation decreased in the contralateral frontal pole during the task state for patients with PSA, and the activation levels negatively correlates with anxiety severities.

ObjectiveTo observe the activation patterns and functional connectivity in the prefrontal cortex of patients with post-stroke anxiety (PSA) using functional near-infrared spectroscopy, in order to explore the underlying neural mechanism. MethodsFrom December, 2024 to September, 2025, 120 stroke patients were selected in Changzhou De'an Hospital. They were divided into PSA group (n = 60) and non-PSA group (n = 60) according to the score of Hamilton Anxiety Scale (HAMA). All patients wore an 18-channel fNIRS acquisition cap for detection. The differences in resting-state functional connectivity between the frontopolar cortex (FPC) and dorsolateral prefrontal cortex (DLPFC) were examined in both groups, as well as task-related activation in these brain regions. ResultsResting-state functional connectivity analysis revealed no statistically significant difference in network connectivity between two groups in the FPC and DLPFC regions (|t| < 1.301, P > 0.05). Task-related activation results revealed significantly reduced activation in the contralateral FPC of PSA group compared to the non-PSA group (Z = -2.063, P < 0.05). Activation levels in this region showed a negative correlation with the scores of HAMA (ρ = -0.201, P = 0.028). ConclusionActivation decreased in the contralateral frontal pole during the task state for patients with PSA, and the activation levels negatively correlates with anxiety severities.

ObjectiveTo observe the activation patterns and functional connectivity in the prefrontal cortex of patients with post-stroke anxiety (PSA) using functional near-infrared spectroscopy, in order to explore the underlying neural mechanism. MethodsFrom December, 2024 to September, 2025, 120 stroke patients were selected in Changzhou De'an Hospital. They were divided into PSA group (n = 60) and non-PSA group (n = 60) according to the score of Hamilton Anxiety Scale (HAMA). All patients wore an 18-channel fNIRS acquisition cap for detection. The differences in resting-state functional connectivity between the frontopolar cortex (FPC) and dorsolateral prefrontal cortex (DLPFC) were examined in both groups, as well as task-related activation in these brain regions. ResultsResting-state functional connectivity analysis revealed no statistically significant difference in network connectivity between two groups in the FPC and DLPFC regions (|t| < 1.301, P > 0.05). Task-related activation results revealed significantly reduced activation in the contralateral FPC of PSA group compared to the non-PSA group (Z = -2.063, P < 0.05). Activation levels in this region showed a negative correlation with the scores of HAMA (ρ = -0.201, P = 0.028). ConclusionActivation decreased in the contralateral frontal pole during the task state for patients with PSA, and the activation levels negatively correlates with anxiety severities.

Objective:To investigate the application value of intraoperative electrocochleography（ECochG） monitoring technique and insertion techniques in cochlear implant（CI） and analyze its relationship with postoperative residual hearing（RH） preservation. Methods:Thirty-one patients（35 ears） who received CI in our hospital from June 2022 to July 2024 were enrolled. The Advanced Bionics Active Insertion Monitoring（AIM） system was used for real-time ECochG monitoring during surgery. Intraoperative cochlear microphonics （CM） waveform changes were recorded and analyzed in relation to postoperative RH preservation. Results:①ECochG recordings were successfully obtained in 34 of 35 ears （97.1%）. ②According to Harris classification, there were 7 ears（20.6%） of Type A（rising）, 7 ears（20.6%） of Type C（declining）, 8 ears（23.5%） of Type CC（fluctuating）, and 12 ears（35.3%） of Type D（no response）. ③The total CM amplitude decrease was significantly moderately correlated with postoperative low-mid frequency hearing loss（r=0.67, P=0.017）. The total CM amplitude decrease was significantly moderately correlated with postoperative low frequency hearing loss（r=0.65, P=0.023）. ④For the mean amplitude variation, the Amax was 30.70 μV, the Amin was 8.64 μV, and the Aend was 18.27 μV. ⑤Sixteen cases completed postoperative follow-up, with an average low-mid frequency（125-1 000 Hz） residual hearing loss of 15.25 dB HL and a RH preservation rate of 87.5%. Conclusion:Intraoperative ECochG monitoring can effectively predict postoperative residual hearing changes, effectively guide surgical manipulation, and improve residual hearing preservation rate.
Humans ; Cochlear Implantation/methods* ; Audiometry, Evoked Response ; Cochlear Implants ; Male ; Female ; Adult ; Middle Aged ; Monitoring, Intraoperative ; Adolescent ; Young Adult ; Minimally Invasive Surgical Procedures ; Child ; Aged ; Postoperative Period

Objective To review the influence of 131I therapy on bone mineral density (BMD) in patients with hyperthyroidism.Methods Published articles of prospective randomized controlled study,clinical controlled study or case-control study on BMD change in patients with hyperthyroidism after 131I therapy were selected from PubMed,the Excerpta Media Database (Embase),Cochrane library,Chinese Journal Full-text Database,Wanfang Database,Vip Database and Chinese Biomedical Literature Database.Data from the date of database establishment to October 2015 were all reviewed.The languages were restricted to English and Chinese.Meta-analysis was performed with RevMan 5.3.Results Thirteen trials with a total of 668 hyperthyroidism patients were included.The meta-analysis showed that BMD of the lumbar spine,hip joint,femoral neck and osteocalcin were significantly improved after 131I therapy.The weighted mean difference (WMD) for BMD of the lumbar spine was 0.07 (95％ CI:0.04-0.11),P=0.O00 2;that of the hip joint and the femoral neck was 0.13(95％ CI:0.09-0.16) and 0.05(95％ CI:0.03-0.06),respectively(both P＜0.01).The standardized mean difference (SMD) of osteocalcin was-1.20(95％ CI:-1.43--0.97) with P＜0.01.Furthermore,the improvements were time dependent within the 2 years' follow-up.Conclusions 131I therapy improves the BMD and osteocalcin in patients with hyperthyroidism in a time dependent manner within 2 years' follow-up.

Objective To explore the role of microRNA-206 (miR-206) in peripheral blood mononuclear cells (PBMCs) in infantile bronchiolitis caused by respiratory syncytial virus (RSV).Methods Thirty-five cases of infantile bronchiolitis and 25 cases of healthy controls were enrolled into the current study.PBMCs were isolated from the peripheral blood of both healthy subjects and those with infantile bronchiolitis in the acute and the convalescent stages.Total RNAs were extracted from PBMCs which were stimulated by phorbol-12-myristate-13-acetate (PMA) and Ionomycin, and then the RNA was transcribed reversely into cDNA.The expressions of miR-206 and Kruppel-like transcription factor 4 (KLF4) were detected by real-time quantitative polymerase chain reaction (qRT-PCR) method.Plasma interleukin-17 (IL-17) was determined by enzyme linked immunosorbent assay (ELISA).Results There was a significant difference in miR-206 levels of children with RSV bronchiolitis in the acute stage(0.055 ±0.018) and the convalescent stage(0.187 ±0.069) as well as the healthy controls(0.204 ± 0.075).Through pairwise comparison, the miR-206 levels in the children in the acute stage were significantly lower than those in the convalescent stage and healthy control group (P ＜ 0.01), but no statistical significance was found between the convalescent stage group and healthy control group(P ＞ 0.05).The levels of KLF4 mRNA of children in the acute stage,convalescent stage as well as the healthy subjects were 0.588 ± 0.161,0.086±0.024,0.075 ±0.019, respectively,which was significantly difference (P ＜ 0.01).The levels of IL-17 were (58.26 ±25.88) ng/L, (9.87 ± 3.01) ng/L, (7.65 ± 2.16) ng/L, respectively (P ＜ 0.01).Compared to the convalescent and the normal control group,both the KLF4 mRNA and IL-17 levels were markedly higher in the acute stage (P ＜ 0.01), but there were no significant differences between children with RSV bronchiolitis in convalescent stage and in the healthy controls (P ＞ 0.05).Furthermore, the result of this study showed a negative correlation between the expression of miR-206 and KLF4(r =-0.624 ,P ＜0.01)and IL-17 (r =-0.609 ,P ＜0.01) in children in the acute stage and a positive correlation between KLF4 mRNA and IL-17 in children in the acute stage (r =0.662, P ＜ 0.01).Conclusion The levels of miR-206 may play a role in the onset of RSV associated post-bronchiolitis (PB) and the low expression of miR-206 in children infected with RSV may increase the susceptibility to PB.

Objective To explore the role of miR-206 in peripheral blood mononuclear cells (PBMCs) of systemic lupus erythematosus (SLE) patients.Methods Human PBMCs were isolated by standard densitygradient centrifugation over Ficoll-Hypaque solution in SLE and healthy controls.Total RNAs were extracted from PBMCs which were stimulated by PMA and ionomycin,thenthe RNA was transcribed reversely into cDNA.The expression of miR-206 and Kruppel-like factor 4 (KLF4) and the orphan nuclear receptor RORγt mRNA was detected by real-time quantitative polymerase chain reaction (qRT-PCR) method.T test and Spearman's correlation test were used for statistical analysis.Results The expression of miR-206 in the PBMCs of SLE patients was significantly decreased compared with that of healthy controls (0.066±0.021 vs 0.143±0.059,t=3.136,P＜0.01).The levels of KLF4 and RORγt mRNAin the PBMCs of SLE patients were increased significantly than those of healthy controls (0.637 ±0.186 vs 0.104 ± 0.028,t=6.673,P＜0.01),(0.575±0.263 vs 0.065±0.014,t=7.386,P＜0.01).Furthermore,there was a negative correlation between the expression of miR-206 and KLF4 or RORγt mRNA in SLE patients (r=-0.627,P＜ 0.01),(r=-0.853,P＜0.01).Conclusion These results indicate that the augmented expression of KLF4 mRNA may be caused by the attenuated expression of miR-206,and the high level of KLF4 mRNA evokes the proportion of Thl7 cells in SLE patients.

s: Objective To explore the role of microRNA-206 in peripheral blood mononuclear cells (PBMC) in the pathogenesis and development of childhood asthma. Methods Twenty-seven asthmatic children and 25 healthy controls were enrolled in the study. Peripheral blood mononuclear cells were isolated in both healthy subjects and asthmatic children in acute attack and remission stages. Total RNAs were extracted from PBMC stimulated by PMA and ionomycin, and then the RNA was reversely transcribed into cDNA. The expressions of microRNA-206 and Kruppel-like factor 4 (KLF4) and IL-17 mRNA were detected by real-time quantitative PCR (qRT-PCR) method. Results There was signiifcant difference of microRNA-206 levels among asthmatic children in attack stage and in remission stage and normal controls (F=46.58~72.81, P=0.000). Through pair-wise comparison, the microRNA-206 levels of asthmatic children in attack stage were signiifcantly lower than those in remission stage and normal control groups (P<0.01). The KLF4 and IL-17 mRNA levels of asthmatic children in attack stage were signiif-cantly higher than those in remission stage and normal control groups (P<0.01). There was no signiifcant difference of miR-206, KLF4 and IL-17 mRNA between asthmatic children in remission stage and the healthy controls (P>0.05). Furthermore, a negative correlation was found between the expression of miR-206 and KLF4 (r=–0.66, P<0.01) and between the expression of miR-206 and IL-17 mRNA (r=–0.81, P<0.01) in asthmatic children in attack stage. A positive correlation was also found between KLF4 and IL-17 mRNA in asthmatic children in attack stage (r=0.70, P<0.01). Conclusions The expression of miR-206 is decreased in asthmatic children, and miR-206 might be involved in the pathogenesis and development of asthma.

Objectives To explore the role of CD4+T cell-derived leptin in peripheral blood mononuclear cells (PBMC) in asthmatic children. Methods Peripheral blood mononuclear cells were isolated from peripheral blood of both healthy subjects and asthmatic children in attack and remission stages. CD4+T cells were purified from PBMCs by mag-netic beads and were cultured in vitro. Supernatants were used to detect the levels of leptin by ELISA. The expression of the orphan nuclear receptor (ROR)γt was detected by real-time quantitative PCR (qRT-PCR) method. Results There was significant difference in CD4+T cell-derived leptin levels of asthmatic children in attack stage (68.46±13.08 pg/ml), remis-sion stage (36.73±6.13 pg/ml) and normal controls (32.82±5.79 pg/ml) (P<0.01). Through pairwise comparison, the leptin levels in children in attack stage were significantly higher than those in remission stage and normal control groups (P<0.01). But no statistical significance was found between remission stage group and normal controls (P>0.05). The plasma leptin of children in attack stage and remission stage, as well as in normal subjects were 16.64 ± 3.53, 14.91 ± 3.24 and 13.72 ± 5.79 ng/ml respectively with no significant differences (P>0.05). The levels of RORγt mRNA were 0.341 ± 0.175, 0.089±0.028 and 0.068±0.018 in children with asthma during attack stage, remission stage and in normal children respec-tively (P<0.01). Compared to remission and normal control groups, the RORγt mRNA level of children in attack stage was markedly higher (P<0.01), but there was no significant difference between asthmatic children in remission stage and the healthy controls (P>0.05). Furthermore, the result of this study showed CD4+T cell-derived leptin positively correlated to RORγt in asthmatic children in attack stage (r=0.681, P<0.01). Conclusions CD4+T cell-derived leptin is elevated in asthmatic children in attack stage and its level is closely related to the pathological process of asthma.