ObjectiveTo investigate the characteristics of gray matter structure and clinical symptoms in patients with Alzheimer's disease （AD） comorbid with apathy （AD-A）. MethodsThe study included 30 patients with AD-A， 30 AD disease patients without apathy （AD without apathy， AD-NA）， and 30 healthy controls （HCs） matched in gender， age， and years of education. All participants underwent a comprehensive neuropsychological assessment and magnetic resonance imaging （MRI） scans. Voxel-based morphometry （VBM） was used to analyze changes in gray matter volume among the three groups. Additionally， the correlation between the identified abnormal brain regions and apathy scale scores was analyzed. ResultsThere were no statistically significant differences among the three groups in terms of age， gender， years of education， or total intracranial volume. Compared with the HCs group， both the AD-A and AD-NA groups showed significantly lower scores in cognitive function （P<0.001）. The AD-A group exhibited significantly higher apathy scale scores compared with the AD-NA group （P<0.001）. Compared with the AD-NA group， the AD-A group showed reduced gray matter volume in the bilateral caudate nucleus， left orbitofrontal cortex， lingual gyrus， inferior frontal gyrus， superior frontal gyrus， entorhinal cortex， right middle frontal gyrus and posterior cingulate cortex （FWE-corrected， P<0.05 for all）. Compared with the HCs group， the AD-A group exhibited reduced gray matter volume in the bilateral middle temporal gyrus， left fusiform gyrus， calcarine sulcus， postcentral gyrus， right inferior frontal gyrus and supramarginal gyrus （FWE-corrected， P<0.05 for all）. Compared with the HCs group， the AD-NA group showed reduced gray matter volume in the left precuneus， inferior temporal gyrus， and right inferior temporal gyrus （FWE-corrected， P<0.05 for all）. In the AD-A group， changes in the gray matter volume of the left caudate nucleus （r= -0.557， P=0.002） and right middle frontal gyrus （r=-0.620， P=0.001） were negatively correlated with the apathy evaluation scale （AES） scores. ConclusionPatients in the AD-A group exhibited significant atrophy in the frontal-temporal-basal ganglia circuit， and the degree of gray matter atrophy was correlated with the severity of apathy.

Total laryngectomy is a crucial surgical intervention for patients with advanced malignant tumors of the larynx and nasopharynx. Despite its effectiveness, this procedure permanently severs the connection between the nasal cavity and the lower respiratory tract, leading to the cessation of nasal airflow. This disruption significantly impairs the patient's sense of smell and adversely affects their quality of life. Although olfactory loss is common in these patients, the assessment and rehabilitation of their olfactory function are often overlooked. This article reviews relevant literature on evaluating olfactory function and rehabilitation methods following total laryngectomy, with the aim of providing a theoretical foundation to enhance olfactory rehabilitation and overall quality of life for these patients.
Humans ; Laryngectomy/rehabilitation* ; Quality of Life ; Smell ; Laryngeal Neoplasms/surgery* ; Olfaction Disorders/etiology*

OBJECTIVES: To investigate the inhibitory effect of multimerin-2 (MMRN2) overexpression on growth and metastasis of cutaneous melanoma cells. METHODS: Clinical data of patients with cutaneous melanoma were obtained from the GEO database to compare MMRN2 expressions between normal and tumor tissues. A protein-protein interaction network was constructed using the STRING database, and the intersecting genes from GEPIA2.0 were subjected to GO and KEGG enrichment analysis. The prognostic relevance of MMRN2 expression level was assessed using Cox regression and "timeROC". The correlations of MMRN2 expression level with immune infiltration and angiogenesis-related genes were analyzed using GSCA database and the ssGSEA algorithm. Colony-forming assay, Transwell assay, and wound healing assay were used to examine the changes in proliferation and migration of cultured cutaneous melanoma cells following MMRN2 knockdown. In a mouse model bearing cutaneous melanoma xenograft, the effect of MMRN2 knockdown on vital organ pathologies, survival of the mice and GM-CSF, CXCL9, and TGF‑β1 protein expressions were analyzed. RESULTS: MMRN2 was significantly upregulated in metastatic cutaneous melanoma (P<0.001). Protein interaction network analysis identified 15 intersecting genes, which were enriched in endothelium development and cell-cell junctions. In patients with cutaneous melanoma, a high MMRN2 expression was correlated with a poor prognosis, an advanced T stage, a greater Breslow depth, and ulceration (P<0.05). MMRN2 expression level was strongly correlated with 24 immune cell types (P<0.001), fibroblasts, endothelial cells, and expressions of the pro-angiogenic genes (KCNJ8, SLCO2A1, NRP1, and COL3A1; P<0.001). In cultured B16F10 cells, MMRN2 knockdown significantly suppressed cell proliferation, migration and invasion and caused remo-deling of the immunosuppressive microenvironment. CONCLUSIONS MMRN2 overexpression drives progression of cutaneous melanoma by enhancing tumor metastasis, angiogenesis and immune evasion, highlighting its potential as a therapeutic target for melanomas.
Humans ; Melanoma/metabolism* ; Animals ; Cell Movement ; Prognosis ; Skin Neoplasms/metabolism* ; Mice ; Cell Proliferation ; Neoplasm Invasiveness ; Cell Line, Tumor ; Protein Interaction Maps

Objective:To explore the correlations between the cerebral infarction area and cytokines and immune status in patients with acute ischemic stroke,and to provide the theoretical basis for immunotherapy of the patients with different degrees of cerebral infarction.Methods:Sixty-seven patients with acute ischemic stroke within 72 h of the onset were randomly selected according to the inclusion and exclusion criteria,and were divided into large-area cerebral infarction group(n=34)and non-large-area cerebral infarction group(n=33)on the basis of the biggest infarction area in the sequences of magnetic resonance diffusion-weighted imaging(CDWI).Clinical baseline characteristics such as gender,age,and medical history were collected from the patients in two groups,the serum levels of interleukin(IL)-2,IL-6,IL-10,and IL-17A,tumor necrosis factor-α(TNF-α),and interferon-γ(IFN-γ)were measured using flow cytometry;the absolute values of lymphocytes(LYM#),lymphocyte percentages(LYM％),and neutrophil/lymphocy ratios(NLR)in peripheral blood of the patients caiculated,and the ratios of IFN-γ/IL-4,TNF-α/IL-4,and TNF-α/IL-10 rations were also calculated.The values of National Institutes of Health Stroke Scale(NIHSS)scores of the patients were evaluatd on the basis of the assessment of clinical neurological signs.The correlations of the cerebral infarction area and NIHSS score,cytokines and immune status groups of the patients in two were tested by rank correlation analysis.Results:Compared with non-large-area cerebral infarction group,the serum levels of IL-2,IL-6,IL-10,IL-17A,TNF-α,and IFN-γ as well as the NLR in the peripheral blood of the patients in large-area cerebral infarction group were significantly increased(P＜0.01),while the LYM#,LYM％and TNF-α/IL-4 were significantly decreased(P＜0.01).There was a positive correlation between cerebral infarction area and NIHSS score in the patients in large-area cerebral infarction group(rs=0.521,P＜0.05),and there was a significantly positive correlation between cerebral infarct area and NIHSS score in the patients in non-large-area cerebral infarction group(rs=0.721,P＜0.001).The NIHSS scores were positively correlated with serum IL-6(rs=0.306,P=0.005),IL-4(rs=0.252,P＜0.001),IL-2(rs=0.109,P=0.025),IL-17A(rs=0.405,P＜0.001),and IFN-γ(rs=0.146,P＜0.001)levels in two groups;no correlations were found between NIHSS scores and TNF-α(rs=0.039,P=0.726)and IL-10(rs=0.121,P=0.192)levels.NIHSS scores of the patients in two groups had negative correlatious with the serum level of LYM#(rs=-0.026,P=0.036)and LYM％(rs=-0.008,P=0.002),and had positive correlated with NLR(rs=0.315,P=0.009).Conclusion:The infarction area of the patients with actue cerebral infarction is correlated with the NIHSS score,the inflammatory response,the degree of adaptive immune injury,and the immune status.The have positive correlation with cytokines and immune markers and the overall size of the infarction area.Compared with the patients with non-large-acea cerebral infarction,the immunosuppression of the patients with large-area infarcted areas is more likely to occure.

This article summarizes the nursing experience of a patient who underwent percutaneous transluminal septal branch microsphere embolization combined with MitraClip surgery.Nursing key points:before the operation,a multidisciplinary case nursing team was established to jointly optimize the surgical risk plan;checklist-based nursing management was adopted to fully implement preoperative preparations;dynamic psychological assessment was conducted and early psychological intervention was carried out.Intraoperative monitoring and prevention of complications were well implemented.Postoperative care:close monitoring of cardiac function;good volume management to maintain electrolyte balance;implementation of risk management for bleeding or thrombosis;enhanced care for urethral bleeding.The patient was discharged 11 days after the operation and followed up for 3 months.The 6-minute walk distance increased from 240 m before the operation to 560 m,and the patient returned to normal life.

Alzheimer′s disease is a serious neurodegenerative disorder. Approximately 80% to 90% of patients are accompanied by behavioral and psychological symptoms of dementia (BPSD), which manifest as a series of behavioral, psychological and mental abnormalities. These abnormalities can accelerate the cognitive deterioration and premature death of patients, and thus are regarded as important clinical symptoms. However, the pathogenesis of BPSD is still unknown, and treatment methods are limited. The pathogenesis of BPSD from the perspective of neuroimaging and pathophysiology, and possible treatment measures were analyzed in this article, in order to provide references for the early diagnosis and treatment of BPSD.

BACKGROUND:The condyle is the most important anatomical structure of the maxillofacial region,and it plays an important role in mastication and articulation of the human body,and its developmental process is quite different from that of the general bone tissues.Abnormal development of the condylar cartilage can lead to various temporomandibular joint disorders to varying degrees,which affects the patient's quality of life.Abnormal conduction of Notch signaling not only influences the developmental process of the condylar cartilage,but also leads to a series of related diseases such as temporomandibular joint disorders.Aberrant Notch signaling not only affects condylar cartilage development and formation,but also leads to a series of related diseases such as temporomandibular joint disorders.However,the role of Notch signaling pathway in condylar cartilage development and temporomandibular joint disorders has not been fully elucidated.OBJECTIVE:To deeply investigate the mechanism of Notch and condylar cartilage growth and development,and discuss the core of Notch as a therapeutic target for temporomandibular joint arthritis.METHODS:We retrieved,searched and screened relevant literature in CNKI and PubMed with the keywords"Notch signaling pathway,condylar chondrocyte,condylar cartilage,temporomandibular arthritis"in Chinese and English respectively to provide a theoretical basis for the full text.Using comparative analysis method,we compared the retrieved literature,excluded the literature with similar content,compared the differences between the screened literature,and selected the content needed for this article,providing the theoretical basis for the writing of the article.By further studying and analyzing the screened literature,the mechanism of action between the factors was clarified to provide a clear idea for the article.A total of 1 848 relevant papers were retrieved and 53 papers were finally included for review.RESULTS AND CONCLUSION:(1)The condylar cartilage grows and develops in a more complex manner than other bones,and it undergoes an endochondral osteogenesis.Condylar chondrocyte differentiation is susceptible to a variety of factors,which ultimately affects the formation of cartilage and osteoblasts.(2)The Notch signaling pathway has attracted much attention in recent years,and plays a very important role in condylar growth and development.(3)The Notch signaling pathway consists of four components:four Notch receptors(Notch 1-4),five Notch ligands(JAG 1/2 and DLL 1/3/4),intracellular transcription factors(CSL-binding proteins),and multiple target genes such as Hes and Hey.The Notch signaling pathway is divided into two main pathways:typical pathway and atypical pathway.(4)The Notch signaling pathway is interfered with by factors such as y-secretase inhibitors or parathyroid hormone-related proteins in vivo,and common factors such as receptors and ligands are expressed abnormally,thus affecting condylar cartilage growth and development.(5)In addition to the various factors in the body,abnormal masticatory stress and excessive loading of the temporomandibular joint can also affect the normal transmission of the Notch signaling pathway,resulting in the abnormal development of the condylar cartilage.(6)The Notch signaling pathway also affects temporomandibular joint arthritis,and the abnormal signaling can affect the pathogenesis of temporomandibular joint arthritis.

Alzheimer's disease (AD) is a progressively worsening neurodegenerative disorder primarily characterized by cognitive dysfunction, which increasingly impairs patients' quality of life as the condition worsened.Recent studies have found that the cerebellum not only plays a crucial role in motor coordination but also is key in learning, memory and executive functions.However, the mechanisms of the cerebellum influences cognitive function in AD patients remain unclear, and further research is needed to elucidate these processes in greater depth.This article reviews the latest research advances on the cerebellum and AD-related cognitive dysfunction, and explores the role of the cerebellum in the pathogenesis, clinical manifestations, and potential treatment strategies for AD, in order to provide valuable insights for future investigations into the pathological mechanisms and clinical therapies of AD.

Alzheimer's disease (AD) is a progressively worsening neurodegenerative disorder primarily characterized by cognitive dysfunction, which increasingly impairs patients' quality of life as the condition worsened.Recent studies have found that the cerebellum not only plays a crucial role in motor coordination but also is key in learning, memory and executive functions.However, the mechanisms of the cerebellum influences cognitive function in AD patients remain unclear, and further research is needed to elucidate these processes in greater depth.This article reviews the latest research advances on the cerebellum and AD-related cognitive dysfunction, and explores the role of the cerebellum in the pathogenesis, clinical manifestations, and potential treatment strategies for AD, in order to provide valuable insights for future investigations into the pathological mechanisms and clinical therapies of AD.

BACKGROUND:The condyle is the most important anatomical structure of the maxillofacial region,and it plays an important role in mastication and articulation of the human body,and its developmental process is quite different from that of the general bone tissues.Abnormal development of the condylar cartilage can lead to various temporomandibular joint disorders to varying degrees,which affects the patient's quality of life.Abnormal conduction of Notch signaling not only influences the developmental process of the condylar cartilage,but also leads to a series of related diseases such as temporomandibular joint disorders.Aberrant Notch signaling not only affects condylar cartilage development and formation,but also leads to a series of related diseases such as temporomandibular joint disorders.However,the role of Notch signaling pathway in condylar cartilage development and temporomandibular joint disorders has not been fully elucidated.OBJECTIVE:To deeply investigate the mechanism of Notch and condylar cartilage growth and development,and discuss the core of Notch as a therapeutic target for temporomandibular joint arthritis.METHODS:We retrieved,searched and screened relevant literature in CNKI and PubMed with the keywords"Notch signaling pathway,condylar chondrocyte,condylar cartilage,temporomandibular arthritis"in Chinese and English respectively to provide a theoretical basis for the full text.Using comparative analysis method,we compared the retrieved literature,excluded the literature with similar content,compared the differences between the screened literature,and selected the content needed for this article,providing the theoretical basis for the writing of the article.By further studying and analyzing the screened literature,the mechanism of action between the factors was clarified to provide a clear idea for the article.A total of 1 848 relevant papers were retrieved and 53 papers were finally included for review.RESULTS AND CONCLUSION:(1)The condylar cartilage grows and develops in a more complex manner than other bones,and it undergoes an endochondral osteogenesis.Condylar chondrocyte differentiation is susceptible to a variety of factors,which ultimately affects the formation of cartilage and osteoblasts.(2)The Notch signaling pathway has attracted much attention in recent years,and plays a very important role in condylar growth and development.(3)The Notch signaling pathway consists of four components:four Notch receptors(Notch 1-4),five Notch ligands(JAG 1/2 and DLL 1/3/4),intracellular transcription factors(CSL-binding proteins),and multiple target genes such as Hes and Hey.The Notch signaling pathway is divided into two main pathways:typical pathway and atypical pathway.(4)The Notch signaling pathway is interfered with by factors such as y-secretase inhibitors or parathyroid hormone-related proteins in vivo,and common factors such as receptors and ligands are expressed abnormally,thus affecting condylar cartilage growth and development.(5)In addition to the various factors in the body,abnormal masticatory stress and excessive loading of the temporomandibular joint can also affect the normal transmission of the Notch signaling pathway,resulting in the abnormal development of the condylar cartilage.(6)The Notch signaling pathway also affects temporomandibular joint arthritis,and the abnormal signaling can affect the pathogenesis of temporomandibular joint arthritis.