Dry eye disease is a chronic ocular surface disorder of multifactorial origin, characterized by a loss of tear film homeostasis and associated with a range of ocular discomfort symptoms. Growing evidence underscores a significant bidirectional relationship between dry eye and depression: individuals with dry eye disease exhibit a higher prevalence of depressive disorders, and conversely, those diagnosed with depression demonstrate an increased susceptibility to developing dry eye. This interplay is mediated through several pathophysiological pathways, such as chronic inflammation, cerebral functional alterations, gut microbiome dysregulation, and sleep disturbances, which may collectively sustain a vicious cycle. The use of antidepressant therapy introduces further complexity, exerting heterogeneous effects on dry eye—some agents may offer symptomatic relief, whereas others can aggravate ocular surface impairment. The mechanisms responsible for these differential outcomes remain incompletely elucidated and merit further investigation. This review systematically consolidates epidemiological data on the dry eye-depression link, examines potential shared pathological mechanisms, and evaluates current therapeutic options. We propose an integrated management approach that combines conventional dry eye treatments, such as traditional Chinese medicine, electroacupuncture, physical activity and antidepressants—a multimodal strategy that may yield synergistic benefits in alleviating both ocular and affective symptoms, thereby improving overall quality of life. Moving forward, research should focus on deciphering the underlying mechanistic pathways and facilitating the translation of these insights into clinical practice to inform targeted, combined treatment regimens for patients with dry eye and depression.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Objective:To investigate the effects of cryopreservation on the results of nucleic acid detection and culture for Bordetella pertussis in residual culture-positive nasopharyngeal swab specimens, aiming to provide the basis for specimens preservation, transport and centralized detection. Methods:In this cross-sectional study, the residual nasopharyngeal swab specimens which were culture-positive for Bordetella pertussis were collected in the Children′s Hospital, Zhejiang University School of Medicine from January to August in 2022. The specimens were placed at ?20 ℃ and?70 ℃ by random number table method, respectively. Re-detection by culture and PCR for Bordetella pertussis were conducted after these specimens were frozen for 114.3±31.9 days. The specimens were grouped according to the cryopreservation temperature and the semi-quantitative results by bacteria culture. The positive rates of the results were compared with χ 2 test between groups. Results:A total of 244 nasopharyngeal swabs specimens were included and 166 were culture-positive after cryopreservation, the positive rate decreased by 32%. Among them, the positive rate of re-culture of specimens containing low bacterial loads decreased by 56% after cryopreservation. However, there was no significant difference in the positive rate of culture between the specimens freezing at ?70 ℃ and ?20 ℃ (χ2=1.65, P=0.20). The positive rate of DNA detection decreased by 10.6% (88.9% vs 78.3%) after cryopreservation. The positive rate of the ?70 ℃ storage group was significantly higher than that of the ?20 ℃ group (χ2=5.11, P=0.02). The positive rate of the re-detection of DNA of nasopharyngeal swabs with low bacteria loads in ?70 ℃ storage group was significantly higher than that of the ?20 ℃ group (χ2=4.86, P=0.03). While for the samples with a bacterial load of "+" or more, there was no significant difference in the positive rate of DNA detection after cryopreservation between the ?20 ℃ and -70 ℃ (χ2=1.25, P=0.26) groups. The positive rate of nasopharyngeal swab culture after cryopreservation was 68.0% (166/244), which was significantly lower than the DNA detection positive rate of 78.3% (191/244, χ2=6.52, P=0.01). Conclusions:Cryopreservation nasopharyngeal swabs specimens could be used for Bordetella pertussis culture and nucleic acid detection. The bacterial load in the original sample affects the positive detection rate after cryopreservation. Cryopreservation has less influence on the positive rate of the result of nucleic acid detection when compared with culture. Preservation at ?70 ℃ is superior to ?20 ℃.

Objective:To investigate the clinical application value of a novel filter's retraction hook capture technique of pull-assisted method for the endovascular retrieval of conical inferior vena cava (IVC) filters whose hook attached to the wall.Methods:From January 2020 to December 2024, patients with conical filters whose hook attached to the wall admitted at Beijing Jishuitan Hospital were enrolled consecutively.Results:A total of 46 patients underwent filter retrieval using filter's retraction hook capture technique of pull-assisted method. Among these patients, 39 cases (84.8%) were successful in filter retrieval, with the penetration distance of cranial anchor vertex of 3.3(2.5, 4.4) mm, and 13 (33.3%) filters were deformed. The other 7 cases were unsuccessful, with a penetration distance of cranial anchor vertex of 5.0 (4.3, 5.0) mm, and 6 (85.7%) filters were deformed. There was a statistically significant difference between the two groups ( P<0.05). One case (2.2%) had IVC injury, one case (2.2%) experienced filter fracture, and no symptomatic pulmonary embolism occurred. Logistic regression analysis showed that filter deformation was an independent dangerous factor for filter's retraction. Conclusions:Filter's retraction hook capture technique of pull-assisted method is effective in removing conical filters whose hook attached to the wall, with no symptomatic PE occurring. This method can be considered as a new adjuvant technique for filter retrieval.

Objective To investigate the electroencephalography(EEG)signal characteristics in patients with neuropathic pain(NP)associated with spinal cord injury(SCI).Methods A total of 90 patients with SCI from January,2018 to November,2023 were selected from the EEG database of the Department of Rehabilitation Medicine,Xijing Hospital,and divided into NP group(n=46)and non-NP group(n=44)according to their symptoms.The resting-state EEG power and reactivity to eye-opening were compared between two groups.Results Compared with non-NP group,EEG power increased in frontal lobe in α and β1 bands,central lobe in δ,θ,α1 and β1 bands,parietal lobe in α and β1 bands,temporal lobe in α and β1 bands,left occipital lobe in α2 band,and occipital lobe in α1 and β1 bands(|Z|>1.998,P<0.05)in NP group during eye-opening;during eye-closing,EEG power increased in prefrontal lobe in α1 and β1 bands,right frontal lobe in θ band,frontal lobe in α and β1 bands,left frontal lobe in β2 band,central lobe in δ,α1 and β1 bands,parietal lobe in α1 and β1 bands,left pari-etal lobe in α2 and β2 bands,right temporal lobe in θ band,temporal lobe in α and β bands,occipital lobe in α1 and β1 bands,and left occipital lobe in β2 band(|Z|>1.970,P<0.05);while the reactivity to eye-opening de-creased in right prefrontal lobe in β1 band,frontal lobe in θ,α and β bands,right central lobe in β1 band,parietal lobe in α1 and β1 bands,right parietal lobe in β2 band,right temporal lobe in δ and θ band,temporal lobe in α1 and β bands,left occipital lobe in α1 band,and occipital lobe in β1(|Z|>1.967,P<0.05).Conclusion Resting-state EEG power characteristically elevates in NP patients after SCI,and the reactivity to eye-open-ing reduces.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Background and Aims:Acute inferior vena cava thrombosis(IVCT)commonly occurs secondary to inferior vena cava filter(VCF)implantation.If not promptly treated,it may lead to serious complications such as bilateral lower limb swelling and pulmonary embolism and can also reduce the likelihood of successful filter retrieval.Percutaneous mechanical thrombectomy(PMT)and catheter-directed thrombolysis(CDT)are currently the main interventional treatments for IVCT,but comparative studies evaluating their efficacy and safety remain limited.This study was to conduct a prospective randomized controlled trial to compare the clinical efficacy and safety of AngioJet mechanical thrombectomy versus conventional CDT in the treatment of acute IVCT and to explore factors influencing filter retrieval rates,thereby providing evidence-based guidance for clinical decision-making.Methods:From January 2022 to December 2024,patients diagnosed with acute IVCT following VCF implantation were prospectively enrolled at the Department of Vascular Surgery,Beijing Jishuitan Hospital,Capital Medical University.Patients were randomly assigned to either the CDT group(n=46)or the PMT group(n=48)according to the interventional procedure used.The two groups were compared in terms of filter retrieval rates,thrombus clearance outcomes,operative time,thrombolytic drug dosage,and incidence of complications.Logistic regression analysis was used to identify factors associated with primary filter retrieval.Results:A total of 94 patients were enrolled,with 46 in the CDT group and 48 in the PMT group.Compared to the CDT group,the PMT group demonstrated a significantly higher primary filter retrieval rate(77.1%vs.43.5%),grade Ⅲ thrombus clearance rate(70.8%vs.37.0%),and better postoperative thrombus scores.Additionally,the PMT group required lower urokinase doses and shorter thrombolysis duration(all P<0.05).The overall filter retrieval rate and 3-month IVC patency were similar between groups,both exceeding 93%.Regarding safety,the CDT group had a higher incidence of catheter-related infections and medical adhesive-related skin injury,while vagal reflex symptoms were more frequent in the PMT group.Logistic regression analysis identified thrombus clearance rate as an independent factor significantly associated with primary filter retrieval in the PMT group(OR=190.773,P<0.05).Conclusion:Compared to CDT,AngioJet mechanical thrombectomy combined with manual aspiration achieves higher thrombus clearance and primary filter retrieval rates in the treatment of acute IVCT while also reducing thrombolysis duration and drug dosage.However,attention should be paid to the increased risk of vagal reflex symptoms.There was no significant difference between the two groups in secondary filter retrieval rates or long-term IVC patency.The choice of intervention should be based on the patient's condition,timing of filter retrieval,and individualized clinical considerations.