BackgroundAnxiety exhibits a rising prevalence among college students. Investigating the mechanisms through which family function relates to anxiety and examining the moderating role of emotion regulation strategies within this context hold substantial implications for promoting mental health among college students. However， existing research has not sufficiently elucidated the complex interplay among family function， emotion regulation， and anxiety among college students. Further research is warranted to clarify the underlying mechanisms linking family function to anxiety outcomes and to examine the potential moderating role of emotion regulation strategies in this causal pathway. ObjectiveTo explore the relationship between family function and anxiety among lower-grade college students， and to validate the moderating role of emotion regulation strategies in this relationship， thereby offering evidence-based insights for anxiety reduction interventions in this population. MethodsIn March 2023， a total of 1 980 first- and second-year students from a comprehensive university in Shanghai were selected using the cluster sampling method. A self-designed demographic questionnaire， the Emotion Regulation Questionnaire （ERQ）， the Family Adaptability and Cohesion Evaluation Scale Ⅱ-Chinese Version （FACES Ⅱ-CV）， and the Symptom Checklist-90 （SCL-90） were utilized for assessment. Pearson correlation analysis and Spearman correlation analysis were employed to test the correlations of each variable. Hierarchical linear regression analysis was conducted to certify the moderating role of emotion regulation strategies in the relationship between family function and anxiety. ResultsCompared with female students， male students scored significantly lower on ERQ cognitive reappraisal （t=-5.793， P<0.01） but significantly higher on ERQ expressive suppression （t=8.359， P<0.01）. For lower-grade college students， scores on adaptability and cohesion subscales of FACES Ⅱ-CV showed a positive association with cognitive reappraisal in ERQ （r=0.251， 0.302， P<0.01）， while simultaneously displaying negative correlations with both expressive suppression in ERQ （r=-0.113， -0.154， P<0.01） and anxiety in SCL-90 （r=-0.243， -0.202， P<0.01）. Notably， anxiety scores in SCL-90 were inversely related to cognitive reappraisal scores in ERQ （r=-0.159， P<0.01） but directly associated with expressive suppression scores in ERQ （r=0.171， P<0.01）. Hierarchical regression analysis indicated that cognitive reappraisal significantly moderated the relationship between family cohesion and anxiety （β=-0.421， P<0.01）. ConclusionThe cognitive reappraisal strategy serves as a moderator in the relationship between family cohesion and anxiety， potentially mitigating the escalation of anxiety levels associated with family dysfunction. ［Funded by Science and Technology Development Fund of Shanghai Pudong New Area （number， PKJ2023-Y21）］

The co-occurrence of diabetes mellitus complicated with depression （DD） is a clinically prevalent comorbidity characterized by complex pathogenesis and challenging therapeutic management， severely impairing patients' quality of life. Recent research indicates that dysregulation in microglia-neuron interaction plays a pivotal role in the pathological progression of DD. Sustained hyperglycemia can activate central microglia， promoting the activation of NOD-like receptor protein 3（NLRP3） inflammasome and the release of abundant pro-inflammatory cytokines， such as interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）， which trigger neuroinflammation. This cascade leads to hippocampal neuronal damage， impaired synaptic plasticity， and neurotransmitter imbalances， ultimately exacerbating depressive-like behaviors. Traditional Chinese medicine （TCM） offers advantages in preventing and treating DD through its multi-component， multi-target， and holistic regulatory approach. TCM can intervene in excessive microglial activation and their aberrant interactions with neurons by modulating neurotrophic signaling pathways such as brain-derived neurotrophic factor （BDNF）/tyrosine receptor kinase B （TrkB）， suppressing neuroinflammation， preserving neuronal structure and function， regulating synaptic plasticity， and improving glucose and lipid metabolism， thereby exerting synergistic therapeutic effects. Focusing on the role of microglia-neuron interaction in the pathological progression of DD， this review systematically elaborates on the research progress of TCM in regulating this interactive process， providing new perspectives and potential targets for the clinical prevention and treatment of DD.

The co-occurrence of diabetes mellitus complicated with depression （DD） is a clinically prevalent comorbidity characterized by complex pathogenesis and challenging therapeutic management， severely impairing patients' quality of life. Recent research indicates that dysregulation in microglia-neuron interaction plays a pivotal role in the pathological progression of DD. Sustained hyperglycemia can activate central microglia， promoting the activation of NOD-like receptor protein 3（NLRP3） inflammasome and the release of abundant pro-inflammatory cytokines， such as interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）， which trigger neuroinflammation. This cascade leads to hippocampal neuronal damage， impaired synaptic plasticity， and neurotransmitter imbalances， ultimately exacerbating depressive-like behaviors. Traditional Chinese medicine （TCM） offers advantages in preventing and treating DD through its multi-component， multi-target， and holistic regulatory approach. TCM can intervene in excessive microglial activation and their aberrant interactions with neurons by modulating neurotrophic signaling pathways such as brain-derived neurotrophic factor （BDNF）/tyrosine receptor kinase B （TrkB）， suppressing neuroinflammation， preserving neuronal structure and function， regulating synaptic plasticity， and improving glucose and lipid metabolism， thereby exerting synergistic therapeutic effects. Focusing on the role of microglia-neuron interaction in the pathological progression of DD， this review systematically elaborates on the research progress of TCM in regulating this interactive process， providing new perspectives and potential targets for the clinical prevention and treatment of DD.

This study investigated the regulatory potential of salidroside (SAL), a primary active compound in Rhodiola rosea L., on osteoclast differentiation by modulating the hypoxia-inducible factor 1-alpha (HIF-1a) pathway in osteoblasts. Luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay were employed to validate whether the receptor activator of nuclear factor-?B ligand (RANKL) is the downstream target gene of HIF-1a in osteoblasts. The study also utilized lipopolysaccharide (LPS)-induced mouse osteolysis to examine the impact of SAL on osteolysis in vivo. Furthermore, conditioned medium (CM) from SAL-pretreated osteoblasts was used to investigate the paracrine effects on osteoclastogenesis through the HIF-1a pathway. Hypoxic condition-induced overexpression of HIF-1a upregulated RANKL levels by binding to the RANKL promoter and enhancing transcription in osteoblastic cells. In vivo, SAL significantly alleviated bone tissue hypoxia and decreased the expression of HIF-1a by downregulating the expression of RANKL, vascular endothelial growth factor (VEGF), interleukin 6 (IL-6), and angiopoietin-like 4 (ANGPTL4). In the paracrine experiment, conditioned media from SAL-pretreated osteoblasts inhibited differentiation through the HIF-1a/RANKL, VEGF, IL-6, and ANGPTL4 pathways. RANKL emerges as the downstream target gene regulated by HIF-1a in osteoblasts. SAL significantly alleviates bone tissue hypoxia and bone loss in LPS-induced osteolysis through the HIF-1a/RANKL, VEGF, IL-6, and ANGPTL4 pathways. SAL inhibits osteoclast differentiation by regulating osteoblast paracrine secretion.
Animals ; Osteoblasts/cytology* ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics* ; Glucosides/administration & dosage* ; Cell Differentiation/drug effects* ; Phenols/administration & dosage* ; Mice ; Osteoclasts/metabolism* ; RANK Ligand/genetics* ; Rhodiola/chemistry* ; Osteogenesis/drug effects* ; Signal Transduction/drug effects* ; Interleukin-6/genetics* ; Male ; RAW 264.7 Cells ; Osteolysis/genetics* ; Humans ; Mice, Inbred C57BL

Objective:To evaluate the clinical efficacy of TCM acupoint application combined with Fuyang cupping in the treatment of chronic bronchitis with lung and kidney yin deficiency syndrome.Methods:A randomized controlled trial study was conducted. From July 2022 to July 2024, 96 patients with chronic bronchitis in our hospital were selected as the observation subjects and divided into two groups using a random number table method, with 48 cases in each group. The control group received treatment with Fuyang cupping, while the study group received treatment with Fuyang cupping and acupoint application. Both groups were treated continuously for 14 days. TCM syndrome scores were performed before and after treatment, and serum TNF-α, CRP, and procalcitonin (PCT) levels were detected using ELISA. Arterial oxygen partial pressure (PaO 2) and carbon dioxide partial pressure (PaCO 2) were measured using a blood gas analyzer. FVC, FEV1, and FEV1 percentage of predicted values (FEV1% predicted value) and maximum expiratory flow (PEF) were measured using a pulmonary function analyzer. The relief time of clinical symptoms such as cough, sputum production, and wheezing during the treatment period were observed and recorded, and the clinical efficacy was evaluated. Results:The total effective rate of the research group was 95.83% (46/48), while that of the control group was 79.16% (38/48), with statistical significance ( χ2=6.10, P=0.013). After treatment, the scores of cough, sputum, wheezing, wheezing, and dry throat and mouth in the study group were lower than those in the control group ( t values were 4.86, 5.89, 5.23, 4.10, 5.49, respectively, P<0.01); PaO 2 level [(95.63 ± 6.45) mmHg vs. (88.44 ± 5.76) mmHg, t=5.76] was higher than of the control group ( P<0.01), and the PaCO 2 level [(40.12 ± 4.28) mmHg vs. (45.63 ± 4.36) mmHg, t=6.25] was lower than of the control group ( P<0.01); the levels of FEV1 [(2.64 ± 0.69) L vs. (1.97 ± 0.74) L, t=4.59], FEV1% predicted value (79.25 ± 11.27 vs. 62.55 ± 10.56, t=7.49), FVC [(3.05 ± 1.04) L vs. (2.06 ± 0.96) L, t=4.85], and PEF [(241.54 ± 19.85) L/min vs. (221.36 ± 19.65) L/min, t=5.01] were higher than those in the control group ( P<0.01); the levels of TNF-α, CRP and PCT in the serum were lower than those in the control group ( t values were 4.39, 6.51 and 18.59, respectively, P<0.001). Conclusion:TCM acupoint application combined with Fuyang cupping can effectively improve the TCM syndrome score and lung function, inhibit inflammatory factor levels, and improve clinical efficacy in chronic bronchitis patients with lung and kidney yin deficiency syndrome.

Multi-family therapy (MFT), as an extension of traditional family therapy, refers to a treatment method in which family members from multiple families participate at the same time. Although its application in severe mental disorders such as schizophrenia is mature, its potential in a wider field and its localization pathway need to be systematically discussed. This paper aims to summarize the development, treatment settings and requirements of the early classic model of MFT, analyze its core mechanism, focus on summarizing the emerging application model variants and effectiveness of MFT in medical care (schizophrenia, eating disorders), school education (refusing to intervene in school) and social work (treating ADHD children, traumatized families, etc.), and comprehensively explore the research methods of effect evaluation.However, there are still some limitations in the current researches, such as lax evaluation, unclear specific action pathway, family vulnerability and lack of cross-cultural adaptability research. Finally, the future development direction is prospected to provide reference for promoting the application practice of MFT.

Objective:To investigate the efficacy and safety of allogeneic hematopoietic stem cell transplantation (allo-HSCT) for the treatment of BCR::ABL-negative chronic neutrophilic leukemia (CNL) and MDS/MPN with neutrophilia.Methods:This study retrospectively analyzed 12 cases of CNL and MDS/MPN with neutrophilia that underwent allo-HSCT from March 2017 to June 2024, comprising 7 males and 5 females with a median age of 48 ( IQR: 28, 59) years. The 2-year overall survival (OS), disease-free survival (DFS), cumulative incidence of relapse (CIR), and transplantation-related mortality (TRM) rates were analyzed. Complications were also assessed. Results:Of the 12 patients, 6 received matched sibling HSCT and 6 received haploidentical HSCT. All patients had successful engraftment, and the median times of neutrophil and platelet engraftment were 17 ( IQR: 11, 24) days and 15 ( IQR: 9, 28) days, respectively. Grade Ⅱ–Ⅳ acute graft versus host disease (GVHD) and chronic GVHD occurred in 2 and 4 cases, respectively. The 2-year OS, DFS, CIR, and TRM rates were (65.6 ± 16.4) %, (41.7 ± 16.6) %, (47.2 ±18.2) %, and (11.1 ± 11.4) %, respectively, after a median follow-up time of 637 ( IQR: 330, 943) days. One patient died from treatment-related complications due to respiratory failure caused by coronavirus disease 2019. Two patients died due to relapse. Conclusion:Allo-HSCT can be applied as a safe and effective approach to treat CNL and MDS/MPN with neutrophilia.

Alzheimer's disease(AD)is an age-related neurodegenerative disease with an increasing incidence worldwide.A large number of studies have shown that the incidence rates of hearing loss is high in patients with mild cognitive impairment and Alzheimer's disease,and may be a risk factor for the occurrence and development of cognitive impairment.There is an interaction between the two,but the causal mechanism is still unclear.Early screening and management of hearing impairment may play an important role in the early diagnosis,symptom im-provement and disease progression of Alzheimer's disease.This paper reviews relevant clinical and basic research to discuss the correlation between hearing loss and Alzheimer's disease,and the possible causal mechanism between them.

Objective To explore the effect and mechanism of Zuogui Jiangtang Jieyu Formula(ZGJTJYF)in treating diabetes-related depression by regulating glutamate receptor 2(GluR2).Methods The primary isolated and cultured hippocampal neurons of SD rats were used.The experiment consisted of normal,model,blank serum(10％blank serum),positive drug(10％[metformin+fluoxetine]drug-containing serum),20％ZGJTJYF group,10％ZGJTJYF group,10％ZGJTJYF+GluR2 knockdown group,and 10％ZGJTJYF+GluR2 overexpression group(with corresponding volume fractions of ZGJTJYF drug-containing serum added).The ZGJTJYF+GluR2 knockdown and overexpression groups,were transfected with lentivirus to obtain hippocampal neurons with either GluR2 overexpression or knockdown.The glucose(150 mmol/L)and corticosterone(200 μmol/L)were used for 18 h to establish an in vitro cell model of hippocampal neurons in diabetes-related depression.After 24 h of successful modeling,the corresponding serum was added to each group for intervention.After 24 h of intervention,the morphological structure of hippocampal neurons was observed using an optical microscope.Biochemical methods were used to determine the glucose and insulin content in cell supernatant.An enzyme-linked immunosorbent assay was used to detect 5-hydroxytryptamine(5-HT)and dopamine(DA)levels in the cell supernatant,and the microtubule-associated protein 1A/1B light chain 3 autophagy double-labeled adenovirus(mRFP-GFP-LC3)autophagy fluorescence double labeling method was used to detect the average fluorescence intensity of LC3 protein in hippocampal neurons.Nissl staining was used to observe synaptic damage in hippocampal neurons,and an immunofluorescence method was used to detect the protein expression of Parkin,phosphatase and tensin homolog-induced putative kinase 1(PINK1),regulating synaptic membrane exocytosis 3(RIMS3),synapsin 1(SYN1),postsynaptic density-95(PSD-95),synapse-associated protein 102(SAP 102),and GluR2 in hippocampal neurons.Realtime fluorescence PCR was used to detect GluR2 mRNA expression in hippocampal neurons,while Western blotting was employed to assess the expression of mitophagy proteins Parkin and PINK1 in these neurons.Results Compared to the normal group,the model group and blank serum group showed structural damage to hippocampal neurons,increased glucose content in cell supernatant,decreased insulin,5-HT,and DA content,increased average fluorescence intensity of LC3,Parkin,and PINK1,decreased average fluorescence intensity of RIMS3,SYN1,PSD-95,SAP 102,and GluR2,decreased GluR2 mRNA expression,increased protein expression of Parkin and PINK1(P＜0.05),and decreased Nissl bodies.Compared to the model group and blank serum group,the above indicators in each administration group were improved to varying degrees(P＜0.05).Compared to the positive drug group,the average fluorescence intensity of LC3,Parkin,and PINK1 decreased,Parkin and PINK1 protein expression decreased,and the average fluorescence intensity of GluR2,SYN1,and PSD-95 increased in 10％ZGJTJYF,20％ZGJTJYF group,and 10％ZGJTJYF+GluR2 overexpression group(P＜0.05).Compared to 10％and 20％ZGJTJYF groups,10％ZGJTJYF+GluR2 knockdown group showed a decrease in 5-HT content,an increase in average fluorescence intensity of LC3 and Parkin,a decrease in average fluorescence intensity of SYN1,PSD-95,and GluR2,a decreased in GluR2 mRNA expression,and an increase of Parkin and PINK1 protein expression(P＜0.05).In contrast,the above indicators were improved to varying degrees in 10％ZGJTJYF+GluR2 overexpression group(P＜0.05).Compared to 10％ZGJTJYF+GluR2 knockdown group,the above abnormal indicators in 10％ZGJTJYF+GluR2 overexpression group were reversed to varying degrees(P＜0.05).Conclusion ZGJTJYF has a protective effect on synaptic damage of hippocampal neurons in diabetes-related depression,and its mechanism may be related to the upregulation of GluR2 and the inhibition of mitophagy over activation.

Objective To explore the effect and mechanism of Zuogui Jiangtang Jieyu Formula(ZGJTJYF)in treating diabetes-related depression by regulating glutamate receptor 2(GluR2).Methods The primary isolated and cultured hippocampal neurons of SD rats were used.The experiment consisted of normal,model,blank serum(10％blank serum),positive drug(10％[metformin+fluoxetine]drug-containing serum),20％ZGJTJYF group,10％ZGJTJYF group,10％ZGJTJYF+GluR2 knockdown group,and 10％ZGJTJYF+GluR2 overexpression group(with corresponding volume fractions of ZGJTJYF drug-containing serum added).The ZGJTJYF+GluR2 knockdown and overexpression groups,were transfected with lentivirus to obtain hippocampal neurons with either GluR2 overexpression or knockdown.The glucose(150 mmol/L)and corticosterone(200 μmol/L)were used for 18 h to establish an in vitro cell model of hippocampal neurons in diabetes-related depression.After 24 h of successful modeling,the corresponding serum was added to each group for intervention.After 24 h of intervention,the morphological structure of hippocampal neurons was observed using an optical microscope.Biochemical methods were used to determine the glucose and insulin content in cell supernatant.An enzyme-linked immunosorbent assay was used to detect 5-hydroxytryptamine(5-HT)and dopamine(DA)levels in the cell supernatant,and the microtubule-associated protein 1A/1B light chain 3 autophagy double-labeled adenovirus(mRFP-GFP-LC3)autophagy fluorescence double labeling method was used to detect the average fluorescence intensity of LC3 protein in hippocampal neurons.Nissl staining was used to observe synaptic damage in hippocampal neurons,and an immunofluorescence method was used to detect the protein expression of Parkin,phosphatase and tensin homolog-induced putative kinase 1(PINK1),regulating synaptic membrane exocytosis 3(RIMS3),synapsin 1(SYN1),postsynaptic density-95(PSD-95),synapse-associated protein 102(SAP 102),and GluR2 in hippocampal neurons.Realtime fluorescence PCR was used to detect GluR2 mRNA expression in hippocampal neurons,while Western blotting was employed to assess the expression of mitophagy proteins Parkin and PINK1 in these neurons.Results Compared to the normal group,the model group and blank serum group showed structural damage to hippocampal neurons,increased glucose content in cell supernatant,decreased insulin,5-HT,and DA content,increased average fluorescence intensity of LC3,Parkin,and PINK1,decreased average fluorescence intensity of RIMS3,SYN1,PSD-95,SAP 102,and GluR2,decreased GluR2 mRNA expression,increased protein expression of Parkin and PINK1(P＜0.05),and decreased Nissl bodies.Compared to the model group and blank serum group,the above indicators in each administration group were improved to varying degrees(P＜0.05).Compared to the positive drug group,the average fluorescence intensity of LC3,Parkin,and PINK1 decreased,Parkin and PINK1 protein expression decreased,and the average fluorescence intensity of GluR2,SYN1,and PSD-95 increased in 10％ZGJTJYF,20％ZGJTJYF group,and 10％ZGJTJYF+GluR2 overexpression group(P＜0.05).Compared to 10％and 20％ZGJTJYF groups,10％ZGJTJYF+GluR2 knockdown group showed a decrease in 5-HT content,an increase in average fluorescence intensity of LC3 and Parkin,a decrease in average fluorescence intensity of SYN1,PSD-95,and GluR2,a decreased in GluR2 mRNA expression,and an increase of Parkin and PINK1 protein expression(P＜0.05).In contrast,the above indicators were improved to varying degrees in 10％ZGJTJYF+GluR2 overexpression group(P＜0.05).Compared to 10％ZGJTJYF+GluR2 knockdown group,the above abnormal indicators in 10％ZGJTJYF+GluR2 overexpression group were reversed to varying degrees(P＜0.05).Conclusion ZGJTJYF has a protective effect on synaptic damage of hippocampal neurons in diabetes-related depression,and its mechanism may be related to the upregulation of GluR2 and the inhibition of mitophagy over activation.