ObjectiveTo investigate the effects of modified Xiaoyaosan （JJXYS） on behavioral abnormalities and hippocampal mitochondrial quality control （MQC） in the rat model of post-myocardial infarction depression （PMD） and preliminarily explore its potential mechanism. MethodsA rat model of PMD was established by left anterior descending coronary artery ligation combined with chronic unpredictable mild stress （CUMS）. Rats were randomized into a control group， a model group， a fluoxetine （FLX， 10 mg·kg^-1） group， and low-， medium-， and high-dose JJXYS （JJXYS-L/M/H， 1.12， 2.24， 4.48 g·kg^-1， respectively） groups. Depressive-like behaviors were evaluated by body weight monitoring， sucrose preference test， open field test， and forced swimming test. Hematoxylin-eosin staining and Nissl staining were used to observe hippocampal histomorphology and neuronal changes. Enzyme-linked immunosorbent assay was conducted to determine the serum levels of 5-hydroxytryptamine （5-HT）， dopamine （DA）， interleukin-1 beta （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-alpha （TNF-α）. The mRNA levels of MQC-related genes including peroxisome proliferator-activated receptor-gamma coactivator-1 alpha （PGC-1α）， nuclear respiratory factor 1 （Nrf1）， and transcription factor A， mitochondrial （TFAM） in the hippocampal tissue were measured by real-time PCR. The expression of proteins related to the dynamin-related protein 1 （Drp1）/PTEN-induced putative kinase 1 （PINK1）/Parkin signaling pathway was determined by Western blot. ResultsCompared with the control group， the model group showed restricted body weight gain， aggravated depressive-like behaviors， declined serum 5-HT and DA levels， evident hippocampal neuronal damage and reduced Nissl bodies， as well as downregulated expression of MQC-related genes and proteins （P<0.05）. Compared with the model group， both FLX and JJXYS alleviated the above changes to varying degrees. Moreover， the JJXYS-M and JJXYS-H groups showed more pronounced effects， improving behavioral performance， restoring 5-HT and DA levels， alleviating hippocampal pathological injury， and upregulating the expression of PGC-1α/Nrf1/TFAM mRNA and Drp1/PINK1/Parkin signaling pathway-related proteins （P<0.05）. ConclusionJJXYS can significantly alleviate depressive-like behaviors and neurotransmitter imbalance in the rat model of PMD by regulating hippocampal MQC and upregulating the Drp1/PINK1/Parkin-related pathway. This study provides experimental evidence for the intervention of PMD with JJXYS.

BackgroundObstructive sleep apnea （OSA） represents a prevalent sleep disordered breathing condition characterized by complex pathophysiology. The arousal threshold （ArTH）， a core non-anatomical contributor to OSA pathogenesis， is intimately tied to the disease severity and clinical phenotypes. To date， research regarding factors associated with ArTH has yielded inconsistent findings， and ArTH profiles and disparities across populations with different genetic backgrounds are not fully elucidated. ObjectiveTo explore the differences of ArTH in OSA patients with different genetic backgrounds and analyze the key factors affecting ArTH， thereby providing evidence for understanding OSA pathophysiology and formulating targeted treatment regimens. MethodsA total of 285 patients who met the diagnostic criteria for OSA， as defined by the Multidisciplinary Diagnosis and Treatment Guidelines for Adult Obstructive Sleep Apnea， were retrospectively enrolled in this study. All participants underwent overnight polysomnography （PSG） at the Sleep Medicine Center of Inner Mongolia Mental Health Center from December 2022 to May 2024. Based on the study design， the cohort was stratified into two distinct genetic background subgroups （group A and group B）. Demographic and clinical characteristics， the Epworth Sleepiness Scale （ESS） score， and overnight PSG data were collected. The apnea hypopnea index （AHI）， the lowest pulse oxygen saturation （LSpO₂）， and fraction of hypopneas （F_Hypopneas） were utilized as surrogate indicators to estimate ArTH in OSA patients. The influencing factors of low ArTH were tested by binary Logistic regression analysis. ResultsAmong the 285 OSA patients， there were 227 cases （79.65%） in group A and 58 cases （20.35%） in group B. Comparisons between the two genetic background subgroups revealed no statistically significant differences in the proportion of low ArTH， ESS score， PSG parameters， and the three markers for low ArTH （AHI<30 events/h， LSpO₂>82.5%， F_Hypopneas>58.3%） （P>0.05）. Binary Logistic regression analysis identified sex （OR=2.421， 95% CI： 1.070–5.478）， BMI （OR=0.847， 95% CI： 0.770–0.932）， N1 sleep duration （OR=0.974， 95% CI： 0.963–0.985）， and hypertension （OR=0.348， 95% CI： 0.143–0.848） as independent factors associated with low ArTH in the total cohort. Stratified analysis by genetic backgrounds revealed that sex（OR=3.799， 95% CI： 1.389–10.392）， BMI（OR=0.819， 95% CI：0.723–0.929）， and N1 sleep duration（OR=0.973， 95% CI： 0.961–0.986） were independent factors of low ArTH in group A. In contrast， only N1 sleep duration （OR=0.951， 95% CI： 0.911–0.993） remained a significant factor in group B. ConclusionArthur may have conservative characteristics in patients with OSA with different genetic backgrounds， but the pathophysiological mechanism of OSA may have population heterogeneity. ［Funded by Inner Mongolia Autonomous Region Natural Science Fundation Project （number， 2024QN08050）； Intra-institutional Scientific Research Project of Inner Mongolia Mental Health Center （number， 2022QNWN0010）］

BackgroundBoth modified Suanzaoren Decoction and estazolam serve as effective treatments for chronic insomnia disorder （CID）. Default mode network （DMN） dysfunction is recognized as the primary pathophysiological mechanism underlying CID. However， it remains unclear whether the two treatments exert their therapeutic effects via convergent modulation of DMN functional connectivity. ObjectiveTo investigate the convergent remodeling characteristics of bidirectional effective connectivity （EC） of core DMN nodes with both the intra-network and the remaining whole-brain regions in CID patients with Yin-deficiency and fire-hyperactivity syndrome following the treatment with modified Suanzaoren Decoction or estazolam， so as to provide neuroimaging evidence for the convergent neural mechanisms underlying the therapeutic effects of both therapies in treating CID. MethodsEighty-two patients diagnosed with CID according to the International Classification of Sleep Disorder， third edition （ICSD-3） were consecutively recruited from the outpatient clinic of the Inner Mongolia Autonomous Region Mental Health Center from October 2020 to September 2023. Based on treatment preference， patients were assigned to receive a 6-week intervention in either the modified Suanzaoren Decoction group （n=52） or the estazolam group （n=30）. Ultimately， 66 patients completed follow-up assessments （modified Suanzaoren Decoction group， n=41； estazolam group， n=25）. All CID patients underwent resting-state functional magnetic resonance imaging scanning before and after treatment. Core DMN nodes including medial prefrontal cortex （mPFC）， bilateral inferior parietal lobule （IPL）， and precuneus （PCUN） were selected as seed regions. Granger causality analysis （GCA） was employed to assess bidirectional EC between the seed regions and both the other intra-DMN nodes and the remaining whole-brain regions. Hepatic and renal function indices were detected pre- and post-treatment to evaluate the safety profiles of both treatments. ResultsAt baseline， significant between-group differences were identified in EC from the left IPL to the left middle fronto-orbital gyrus/gyrus rectus （t=5.24， Z=4.84， voxel-level P<0.001， cluster-level P<0.05， GRF-corrected）， with the modified Suanzaoren Decoction group exhibiting stronger EC than the estazolam group. No significant between-group differences were observed in EC between other core DMN nodes and remaining whole-brain regions （P>0.05）. Within-group pre- to post-treatment comparisons demonstrated consistent connectivity alterations in both groups. Specifically， EC from the left IPL to the supplementary motor area （SMA） decreased after treatment （modified Suanzaoren Decoction group： t=-6.28， Z=5.208； estazolam group： t=-5.58， Z=4.425）. Conversely， EC from the SMA to the left IPL increased （modified Suanzaoren Decoction group： t=5.89， Z=4.968； estazolam group： t=6.15， Z=4.720）. Furthermore， both groups demonstrated reduced EC from the PCUN to the left IPL （modified Suanzaoren Decoction group： t=-5.85， Z=4.94； estazolam group： t=-5.75， Z=4.515）， and elevated EC from the left IPL to the PCUN （modified Suanzaoren Decoction group： t=5.29， Z=4.579； estazolam group： t=4.55， Z=3.826） （voxel-level P<0.001， cluster-level P<0.05， GRF-corrected）. No significant pre- to post-treatment differences were observed in hepatic or renal function indices in either group （P>0.05）. ConclusionIn CID patients with Yin-deficiency and fire-hyperactivity syndrome， both modified Suanzaoren Decoction and estazolam induce convergent bidirectional remodeling of EC between the left IPL and the SMA and the PCUN. ［Funded by Natural Science Fund Project of Inner Mongolia Autonomous Region （number， 2019MS08099）； ClinicalTrials.gov number， NCT06452953］

Objective:To investigate the efficacy and treatment adherence of digital cognitive behavioral therapy for insomnia (dCBT-I) in patients with insomnia disorder accompanied by anxiety and depressive symptoms, and to provide empirical evidence for its clinical application.Methods:From December 2023 to December 2024, 102 patients with insomnia disorder accompanied by anxiety and depressive symptoms were recruited from the outpatient department of Inner Mongolia Brain Hospital and randomly assigned to either the dCBT-I group ( n=56) or the digital sleep hygiene education (dSHE) group ( n=46). The dCBT-I group received a 4-week intervention comprising 5 core modules, while the dSHE group received 4 weeks of digital sleep hygiene education. Both groups received weekly guidance from clinical psychologists. Subjective sleep quality (Insomnia Severity Index, ISI), anxiety (Hamilton Anxiety Scale, HAMA), and depressive symptoms (17-item Hamilton Depression Scale, HAMD 17) were assessed at baseline, week 4, week 8, and week 12. Objective sleep parameters (polysomnography, PSG) and cognitive function (Repeatable Battery for the Assessment of Neuropsychological Status, RBANS) were evaluated at baseline and week 4. Linear mixed-effects model was used to analyze the effects of group, timepoint, and their interaction on outcome measures, after controlling medication history, age, sex, education level, ethnicity, and marital status as covariates. Results:A total of 76 patients (dCBT-I: n=42; dSHE: n=34) completed the 4-week intervention, yielding a treatment adherence rate of 74.5%(76/102). At weeks 4, 8, and 12, the dCBT-I group demonstrated significantly lower scores on the ISI, HAMA, and HAMD 17 scales compared to the dSHE group (β=-1.70--0.66, t=-15.38--6.21, all P<0.05), along with higher rates of medication reduction (χ 2=16.40, 9.22, 6.66, all P<0.05). No significant differences were observed in PSG parameters between the two groups. However, the dCBT-I group demonstrated significant improvements in RBANS subdomains, including immediate memory, language function, and delayed memory (β=0.45, 0.86, 1.43, t=3.09, 2.67, 4.36, all P<0.05). Conclusion:dCBT-I is an effective and well-adhered intervention for patients with insomnia disorder accompanied by anxiety and depressive symptoms, warranting broader clinical implementation.

Kleine-Levin Syndrome(KLS)is a rare neurological disease characterized by recurrent episodes of hypersomnia, hyperphagia, hypersexuality, and cognitive and behavioral abnormalities, with complete functional recovery between episodes. Its pathogenesis remains unclear. We report a 33-year-old female with a 17-year clinical course, characterized mainly by recurrent hypersomnia. During episodes, the patient exhibited prominent anorexia, irritability, derealization, and disorientation, followed by brief periods of excitement after episode resolution. Inter-episode periods were entirely normal. Long-term polysomnography monitoring was conducted for a total of 7 792 minutes. Unlike the typical hyperphagia commonly observed in KLS, this case was marked by prominent anorexia, underscoring the clinical heterogeneity of KLS.This report adds to the limited documentation of rare cases in China.

BackgroundThe functional changes of the default mode network （DMN） are closely related to the onset of major depressive disorders. However， the relationship between the DMN subsystem （core subsystem， dorsomedial prefrontal cortex subsystem， medial temporal lobe subsystem） and symptoms of first-episode major depressive disorder remains unclear. ObjectiveTo investigate abnormal functional connectivity between DMN subsystems and the whole brain in first-episode major depressive disorder patients during the resting-state， and to analyse the correlations between these functional connectivity patterns and clinical symptoms， so as to reveal the potential neural mechanisms from the perspective of DMN subsystem. MethodsFrom September 2020 to September 2023， a total of 64 first-episode outpatients and inpatients meeting the diagnostic criteria for major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders， fourth edition （DSM-IV） were enrolled at the Inner Mongolia Autonomous Region Mental Health Center as the study group. During the same period， 54 healthy volunteers matched for age， gender， and years of education were recruited from the community as the control group. Both groups were assessed using the Hamilton Depression Scale-24 item （HAMD-24）. Resting-state functional magnetic resonance images （rs-fMRI） of the two groups were acquired using a Siemens 3.0 T scanner， and differences in functional connectivity between DMN subsystems （core subsystem， dorsomedial prefrontal cortex subsystem， medial temporal lobe subsystem） and the whole brain were compared. The functional connectivity values of brain regions with statistically significant differences between the two groups were extracted. Spearman's rank correlation coefficient analysis was used to investigate the correlation between these functional connectivity values and HAMD-24 scores of the study group. ResultsUltimately， 46 patients and 43 controls completed the study. Compared with the control group， the study group exhibited significantly stronger functional connectivity in the following pathways： between the right superior parietal lobule （core subsystem） and right cerebellar lobule VIII （t=3.954， P<0.05， GRF-corrected）， between the right lateral temporal cortex （dorsomedial prefrontal cortex subsystem） and right cerebellar lobule VIII， right and left hippocampi， right medial， and paracingulate gyrus （t=4.595， 4.208， 5.200， 4.038， P<0.05， GRF-corrected）， and between the temporoparietal junction （dorsomedial prefrontal cortex subsystem） and left lingual gyrus and right cerebellar lobule VIII （t=3.557， 4.274， P<0.05， GRF-corrected）. Conversely， weaker functional connectivity was observed between the right inferior frontal gyrus and left gyrus rectus （t=-3.824， P<0.05， GRF-corrected）. Furthermore， within the study group， the functional connectivity values between the right lateral temporal cortex and right hippocampus， as well as between the temporoparietal junction and right cerebellar lobule VIII， were both negatively correlated with the HAMD-24 cognitive impairment factor score （r=-0.306， -0.318， P<0.05）. ConclusionIncreased functional connectivity between the DMN （specifically its core and dorsomedial prefrontal cortex subsystems） and cerebellum， partial limbic system， and lingual gyrus may be associated with the neuropathology of first-episode major depressive disorder. Furthermore， alterations in functional connectivity between the dorsomedial prefrontal cortex subsystem and both the cerebellum and hippocampus in these patients may be related to cognitive function. ［Funded by 2019 Annual Inner Mongolia Autonomous Region Natural Science Foundation Project （number， 2019MS03038）； 2023 Annual Inner Mongolia Autonomous Region Natural Science Foundation Project （number， 2023MS08028）］

Objective To investigate whether exposure pathways influence the distribution pattern and toxicity of polystyrene nanoplastics(PSNPs)in hepatic cells.Methods Male C57BL/6J wild-type healthy mice aged 6 to 8 weeks old and weighed 18 to 22 g were administered with PSNPs via gavage or tail vein injection.Then,we tracked PSNPs distribution in the major organs of mice via an in vivo imaging system(IVIS).After that,we analyzed the cellular accumulation patterns in hepatic cell subpopulations(hepatocytes and Kupffer cells)using immunofluorescence and transmission electron microscopy(TEM).300 nm PSNPs were administered via gastric gavage or tail vein injection,and 70 nm PSNPs were injected via the portal vein.The cellular localization of PSNPs in the liver was analyzed using immunofluorescence.Subsequently,using AML-12 cells,a normal mouse liver cell line,as the parenchymal hepatocyte model,the uptake of PSNPs in AML-12 cells was analyzed by confocal laser scanning microscope(CLSM).Flow cytometry was performed to observe and quantify PSNPs uptake,and to analyze the underlying endocytosis mechanisms.IVIS was used to analyze PSNPs uptake features in vivo.Finally,using mouse macrophage line RAW264.7 as a Kupffer cell model and AML-12 cells as a parenchymal hepatocyte model,the cell-type-specific toxic effects induced by 100 μg/ml PSNPs were examined through transcriptomics and metabolomics analyses.Results IVIS revealed predominant hepatic accumulation of PSNPs regardless of exposure pathways via intragastric gavage or tail vein injection.Immunofluorescence/TEM demonstrated exposure pathway-dependent cellular distribution:intragastric PSNPs were localized mainly in hepatocytes,while intravenous PSNPs were accumulated in Kupffer cells.Changes in particle size(300 nm vs.70 nm)did not alter the cellular distribution pattern,while 70 nm PSNPs injected via the portal vein accumulated in Kupffer cells,which suggested that the cell-type-specific distribution of PSNPs in the liver was independent of PSNPs size and might be related to the transport of PSNPs in the gastrointestinal tract.Flow cytometry showed that PSNPs uptake by AML-12 was time-dependent and that the underlying endocytosis mechanism involved pathways mediated by clathrin(P<0.000 1),macropinocytosis(P=0.002 6),and lipid rafts(P<0.000 1).Findings on PSNPs distribution in blood revealed that the uptake of PSNPs by hepatocytes exhibited a rate saturation phenomenon.Multi-omics analysis identified distinct toxicity patterns:PSNPs disrupted lipid metabolism and neurotransmitter homeostasis in AML-12 cells and induced inflammation and oxidative stress in Kupffer cells.Conclusion Exposure pathways mediate the hepatic cell-type-specific distribution of PSNPs,thereby altering the downstream toxicological consequences induced by exposure to PSNPs.

Objective:To investigate the efficacy and treatment adherence of digital cognitive behavioral therapy for insomnia (dCBT-I) in patients with insomnia disorder accompanied by anxiety and depressive symptoms, and to provide empirical evidence for its clinical application.Methods:From December 2023 to December 2024, 102 patients with insomnia disorder accompanied by anxiety and depressive symptoms were recruited from the outpatient department of Inner Mongolia Brain Hospital and randomly assigned to either the dCBT-I group ( n=56) or the digital sleep hygiene education (dSHE) group ( n=46). The dCBT-I group received a 4-week intervention comprising 5 core modules, while the dSHE group received 4 weeks of digital sleep hygiene education. Both groups received weekly guidance from clinical psychologists. Subjective sleep quality (Insomnia Severity Index, ISI), anxiety (Hamilton Anxiety Scale, HAMA), and depressive symptoms (17-item Hamilton Depression Scale, HAMD 17) were assessed at baseline, week 4, week 8, and week 12. Objective sleep parameters (polysomnography, PSG) and cognitive function (Repeatable Battery for the Assessment of Neuropsychological Status, RBANS) were evaluated at baseline and week 4. Linear mixed-effects model was used to analyze the effects of group, timepoint, and their interaction on outcome measures, after controlling medication history, age, sex, education level, ethnicity, and marital status as covariates. Results:A total of 76 patients (dCBT-I: n=42; dSHE: n=34) completed the 4-week intervention, yielding a treatment adherence rate of 74.5%(76/102). At weeks 4, 8, and 12, the dCBT-I group demonstrated significantly lower scores on the ISI, HAMA, and HAMD 17 scales compared to the dSHE group (β=-1.70--0.66, t=-15.38--6.21, all P<0.05), along with higher rates of medication reduction (χ 2=16.40, 9.22, 6.66, all P<0.05). No significant differences were observed in PSG parameters between the two groups. However, the dCBT-I group demonstrated significant improvements in RBANS subdomains, including immediate memory, language function, and delayed memory (β=0.45, 0.86, 1.43, t=3.09, 2.67, 4.36, all P<0.05). Conclusion:dCBT-I is an effective and well-adhered intervention for patients with insomnia disorder accompanied by anxiety and depressive symptoms, warranting broader clinical implementation.

Kleine-Levin Syndrome(KLS)is a rare neurological disease characterized by recurrent episodes of hypersomnia, hyperphagia, hypersexuality, and cognitive and behavioral abnormalities, with complete functional recovery between episodes. Its pathogenesis remains unclear. We report a 33-year-old female with a 17-year clinical course, characterized mainly by recurrent hypersomnia. During episodes, the patient exhibited prominent anorexia, irritability, derealization, and disorientation, followed by brief periods of excitement after episode resolution. Inter-episode periods were entirely normal. Long-term polysomnography monitoring was conducted for a total of 7 792 minutes. Unlike the typical hyperphagia commonly observed in KLS, this case was marked by prominent anorexia, underscoring the clinical heterogeneity of KLS.This report adds to the limited documentation of rare cases in China.

Objective To investigate whether miR-19a interacts with insulin-like growth factor 2 receptors(IGF-2R)in infantile hemangiomas(IHs)and affects the proliferation,migration,and adipogenesis of hemangioma stem cells(HemSCs).Methods HemSCs were isolated,screened and cultured from IH specimens.IGF-2R expression in HemSCs was identified using immunohistochemistry.HemSCs transfected with miR-19a mimics and inhibitors were subjected to CCK-8,wound healing,Transwell,qRT-PCR,and Western blot analyses.Results Compared with the control,the proliferation and migration rate of HemSCs treated with miR-19a inhibitors were significantly increased,and overexpression of miR-19a significantly inhibited IGF-2 induced cell migration and proliferation(P＜0.05).Conclusion MiR-19a may inhibit HemSCs proliferation,migration,and adipogenesis by targeting IGF-2R.