Objective To explore the potential profile of body image and its influencing factors among head and neck cancer patients.Methods Convenience sampling was employed to investigate 335 head and neck cancer patients in a tertiary hospital in Shandong Province from October 2023 to May 2024.Data was collected using the patient's general information questionnaire,Body Image Scale,Medical Coping Modes Questionnaire,Perceived Social Support Scale,Comprehensive Score for Financial Toxicity based on the Patient-Reported Outcome Measures.Latent profile analysis and multivariate Logistic regression analysis were used to explore distinct profiles and influencing factor of body image in head and neck patients.Results A total of 335 valid questionnaires were collected in this study,and 95.4％of the valid questionnaires were included.Body image of patients with head and neck cancer could be divided into 3 latent profiles:body emotional stability(41.5％),body cognitive dissatisfaction(33.7％)and social behavior avoidance(24.8％).Age,location of cancer onset,stage of cancer,surgical treatment,medical coping style(facing coping,yielding coping),social support and economic toxicity were the factors influencing the latent profiles of body image in patients with head and neck cancer(P＜0.05).Conclusion There is heterogeneity in body image of patients with head and neck cancer.Medical staff should implement targeted management strategies based on the influencing factors of different profiles to reduce the body image disorders in patients with head and neck cancer,and to promote patients to better return to society.

Objective To investigate the relationship between extracranial carotid artery tortuosity-related indicators and extracranial internal carotid artery aneurysm(ICAA)in elderly patients with suspected cerebrovascular disease.Methods A retrospective analysis was performed on 124 elderly patients with suspected cerebrovascular diseases undergoing head CT angiography(CTA)in our hospital from January 2021 to December 2023.According to the diagnostic results,they were divided into ICAA group(68 cases)and control group(56 cases).The extracranial carotid artery tortuosity-related indicators were compared between the two groups.Multivariate logistic regression analysis was used to identify the influencing factors for ICAA.ROC curve analysis was employed to analyze the diagnostic value of head CTA parameters for extracranial ICAA,and the area under curve(AUC)was calculated.Results There were no statistical differences in the pro-portions of extracranial internal carotid artery(EICA)without kinking,tortuosity,and coiling be-tween the two groups(P＞0.05).The ICAA group had significantly higher proportion of EICA(32.4％vs 14.3％,P＜0.05),and obviously greater common carotid artery kinking index,EICA kinking index,and internal carotid artery angle than the control group(P＜0.01).Multivariate lo-gistic regression analysis showed that kinking,common carotid artery kinking index,EICA kin-king index,and internal carotid artery angle were influencing factors for ICAA(P＜0.05,P＜0.01).ROC curve analysis indicated that in diagnosing ICAA,the sensitivity and the specificity was 70.59％and 82.14％,respectively,for common carotid artery kinking index,was 83.82％and 87.50％,respectively,for EICA kinking index,and was 80.88％and 83.93％,respectively,for in-ternal carotid artery angle.Conclusion The degree of EICA kinking is correlated with extracranial ICAA,and EICA kinking is more likely to cause ICAA.Head CTA parameters can reflect the morphological features of internal carotid artery kinking and had high adjuvant diagnostic value for diagnosing ICAA.

SPF chickens were immunized with HN-mRNA vaccine by intramuscular injection.He-magglutination inhibition(HI)test,lymphocyte proliferation test,RT-qPCR and pathological sec-tions were used to evaluate the humoral and cellular immunity and protection against challenge in-duced by the candidate HN-mRNA vaccine.The results showed that 2.5,5.0,and 7.5 μg HN-mR-NA induced HI antibody antibodies in a dose-dependent manner.Among them,the Hi antibody in-duced by 7.5 μg HN-mRNA was slightly higher than that of the weak toxic vaccine(La Sota strain).In addition,in response to the stimulation of inactivated NDV virus,the proliferation and activation of lymphocytes in 2.5,5.0 and 7.5 μg HN-mRNA immunization groups and commercial vaccine group were observed.To further evaluate the antiviral protection provided by HN mRNA immunization,the 105 ELD50 NDV strong strain NA-1 was used to attack the 7.5 μg HN-mRNA immunised group and the commercial weakened vaccine(La Sota strain)and PBS groups using na-sal and ocular drops.The results showed that the survival rate of 7.5 μg HN-mRNA immunization group and commercial vaccine group was 100％,and these vaccines could protect tissues and or-gans from the damage caused by virus infection.At the same time,7.5 μg HN-mRNA and commer-cial vaccine could shorten the time of virus shedding in vitro and the viral load in vivo.This study provides a foundational framework for the clinical application of NDV HN mRNA candidate vac-cines and offers insights for the development of novel mRNA vaccines for poultry.

Objective:To analyze the clinical features and diagnostic process of ring chromosome syndrome.Methods:Clinical data of 9 children with ring chromosome syndrome who were treated at the Children′s Medical Center of Peking University First Hospital from September 2009 to May 2025, were summarized and analyzed in a case series study. The data included clinical manifestations, types of epileptic seizures, genetic testing, treatment outcomes, and follow-up results, et al.Results:Among the 9 children with ring chromosome syndrome, there were 6 girls and 3 boys, including 4 children with ring chromosome 20 syndrome, 3 children with ring chromosome 14 syndrome, and 1 child each with ring chromosome 13 and 17 syndrome. All 9 children had de novo chromosomal variations. Among them, 3 children of ring chromosome 20 syndrome were mosaic, and the remaining 6 children were non-mosaic. All 9 children exhibited diverse clinical features, especially those with ring chromosome 20 syndrome, which presented with specific manifestations. The 4 children with ring chromosome 20 syndrome all had acute epileptic seizures as the initial symptom, with onset ages of 67, 39, 17, and 96 months, and all had focal seizures. One child with ring chromosome 20 syndrome had non-convulsive status epilepticus. Development of all 4 children with ring chromosome 20 syndrome was normal before seizure onset, but 3 children showed regression after onset. No physical deformities were observed in 4 children with ring chromosome 20 syndrome, and 2 children were misdiagnosed, 3 children underwent whole exome sequencing and copy number variation analysis in their families, with no abnormalities detected. All 4 children with ring chromosome 20 syndrome were diagnosed through chromosomal karyotype analysis, the intervals between onset and diagnosis were 2, 81, 19 and 13 months, respectively. Follow-up showed that epileptic seizures were not controlled in all 4 children with ring chromosome 20 syndrome. The other 5 children were characterized by developmental delay as the initial symptom, followed by epileptic seizures between 3 and 24 months of age. Developmental regression of the other 5 children did not occur after onset, 2 of them had microcephaly, and 3 had wide-set eyes. No misdiagnoses were reported in these 5 children, and the intervals between onset and diagnosis were 7, 3, 55, 3, and 106 months, respectively. Follow-up showed that epileptic seizures were controlled in these 5 children. Conclusions:Ring chromosome 20 syndrome typically manifest with epilepsy as the initial symptom and are refractory to drug treatment, their early development is entirely normal. Ring chromosome 13, 14, and 17 syndrome are characterized by developmental delay from an early age, followed by the onset of epileptic seizures, which are easily controlled. Conventional whole exome sequencing and copy number variation analysis in families rarely detect ring chromosome abnormalities. Early chromosomal karyotype analysis is essential for the diagnosis of ring chromosome syndrome.

Objective To explore the effectiveness of a hospital-to-home transitional health management program for caregivers of children with severe encephalitis,aiming to provide a reference for optimizing transitional care models for these patients.Methods A convenience sampling method was used to select 84 children with severe encephalitis and their caregivers admitted to the neurology department of a tertiary hospital in Zhengzhou between March 2023 and June 2024.According to the admission time,they were divided into an experimental group and a control group,with 42 cases in each group.The experimental group received a hospital-to-home transitional health management program in addition to routine care,while the control group received standard care and discharge instructions.Differences in caregivers' perceived benefits,caregiver burden,disease management ability,and post-intervention outcomes of the children were compared between the 2 groups before and after the intervention.Results All 42 participants in both groups completed the study.After the intervention,the experimental group reported higher perceived benefits of(91.29±9.76)compared to(84.81±12.86)in the control group,lower caregiver burden of(48.55±7.15)compared to(54.71±11.23)in the control group,greater disease management ability of(41.83±4.97)than(37.79±5.23)in the control group,and lower difficulty in disease management of(31.52±7.82)compared to(34.55±3.96)in the control group,with all differences being statistically significant(P＜0.05).No statistically significant difference was found in the prognosis of the children between the 2 groups(P=0.500).Conclusion The hospital-to-home transitional health management program can effectively enhance caregivers'perceived benefits and disease management capabilities,reduce their caregiving burden,and provide scientific evidence for optimizing transitional care for children with severe encephalitis.

Objective:To summarize the genotype and clinical phenotype characteristics of children with epilepsy associated with the SCN1B gene encoding the sodium channel β1 subunit. Methods:The genotypes and clinical phenotypes of patients with SCN1B variants among suspected genetic epilepsy cases treated at the Children′s Medical Center of Peking University First Hospital between May 2016 and July 2024 were analyzed. These variants were identified using next-generation sequencing and subsequently validated by Sanger sequencing or quantitative polymerase chain reaction methods. Results:A total of 17 patients were analyzed, including 8 males and 9 females. Ten cases of missense variations (including 2 with the same variations), 4 cases of deletion variations, and 1 case each of nonsense variations, splice site variations, and exons 4-5 deletions were identified. Among them, 6 cases had novel SCN1B variations. The variants in 11 cases were inherited from 1 parent. Eleven types of gene variants have not been reported yet. Onset of epilepsy ranged from 3 months to 5 years and 3 months old (median age: 14 months). Types of seizures included generalized tonic-clonic seizures (GTCS) in 14 cases, focal seizures in 9 cases, myoclonic seizures in 3 cases, atypical absence seizures in 2 cases and epilepsy spasms, tonic seizures and atonic seizures in 1 case each. Eleven cases had diverse seizure types. Fourteen cases (14/17) demonstrated fever sensitivity. Electroencephalography revealed focal discharges in 3 cases, coinciding with focal and generalized discharges in 3 additional cases, and multifocal discharges in 6 cases. Seizures were identified in 4 cases: 1 case of myoclonic seizures, 1 case of GTCS, 1 case of atypical absence seizures, and 1 case exhibiting both myoclonic and tonic seizures. Nine cases (9/17) were diagnosed with genetic epilepsy with febrile seizures plus, 1 case diagnosed with myoclonic epilepsy in infancy and 1 diagnosed with infant epileptic spasms syndrome. There were 2 cases of nonspecific developmental epileptic encephalopathy, while the remaining 4 cases could not be diagnosed with a specific epileptic syndrome. Effective antiseizure medications (ASMs) included valproate in 8 cases, levetiracetam in 5 cases, topiramate in 3 cases, clobazam in 2 cases, clonazepam and vigabatrin in 1 case each. Sodium channel blockers exacerbated seizures in 3 cases, specifically oxcarbazepine in 2 cases and lamotrigine in 1 case. At the last follow-up, seizures were controlled for at least 6 months in 14 patients (14/17), while seizures remained uncontrolled in 3 patients despite trialing 2 or more ASMs. Thirteen patients exhibited normal development, while 4 experienced developmental delays. Conclusions:The heterozygous variants in children with SCN1B gene-related epilepsy include missense, deletion, nonsense, splice site variants, and exon deletions. The correlation between different genetic variants and clinical phenotypes remains unclear. These variants are associated with epilepsy onset from infancy to early childhood, presenting with various seizure types, with GTCS being the most common. Phenotypic manifestations can vary significantly in severity, ranging from benign febrile seizures or febrile seizures plus to developmental epileptic encephalopathy. Valproic acid demonstrates the highest effectiveness rate, while the use of sodium channel blockers may worsen seizures in certain patients, necessitating cautious administration.

Objective:To summarize the clinical phenotype and genetic features of patients with relapsing encephalopathy with cerebellar ataxia (RECA) caused by ATP1A3 gene R756 variants. Methods:A retrospective analysis was performed on patients carrying the ATP1A3 gene R756 variants, identified by whole-exome sequencing of family members, at Capital Center for Children′s Health, Capital Medical University and Children's Medical Center, Peking University First Hospital from August 2005 to February 2024. Their clinical, laboratory, neuroimaging, electrophysiological and genetic characteristics were summarized. Results:A total of 13 RECA patients were enrolled in this study, including 8 males and 5 females. The age of onset was 8 months to 5 years, with a median age of onset of 18 months. All of 13 patients presented paroxysmal episodes of neurological decompensations triggered by fever and residual symptoms following the acute phase. During acute attack stage, ataxia was observed in all 13 cases, muscle weakness in 12 cases, dysarthria in 12 cases, altered consciousness in 10 cases, dysphagia in 10 cases, dystonic episodes in 4 cases, abnormal eye movement in 2 cases, choreoathetosis in 2 cases, and epileptic seizures in 1 case. All 13 patients had residual symptoms during the nonparoxysmal period, of whom 9 patients had ataxia, 9 patients had dysarthria, 4 patients had dystonia, 3 patients had cognitive disorders, and 1 patient had epileptic seizures. All 13 cases had ATP1A3 missense variants, and variant c.2266C>T/p.R756C was found in 6 cases, c.2267G>A/p.R756H in 5 cases, and c.2267G>T/p.R756L in 2 cases. Nine cases carried de novo variants, 4 with inherited variants. Conclusions:RECA caused by variants of ATP1A3 in residue 756 typically presents with an acute onset during infancy or early childhood, precipitated by febrile episodes and characterized by recurrent episodes of ataxia, with bulbar paralysis, muscle weakness and altered consciousness. Recurrence is common, and the most common persistent symptoms are cerebellar ataxia and dysarthria. A few patients have cognitive impairment. Three types of ATP1A3 gene variants R756C, R756H and R756L are related with RECA, and R756C is the most common variant.

OBJECTIVES: To explore the molecular mechanism by which lncRNA SNHG15 regulates proliferation, invasion and migration of lung adenocarcinoma cells. METHODS: The lncRNA microarray chip dataset GSE196584 and LncBase were used to predict the lncRNAs that interact with miR-30b-3p, and their association with patient prognosis were investigated using online databases, after which lncRNA nucleolar RNA host gene 15 (SNHG15) was selected for further analysis. The subcellular localization of lncRNA SNHG15 and its expression levels in normal human lung epithelial cells and lung adenocarcinoma cell lines were detected using fluorescence in situ hybridization and qRT-PCR. In cultured A549 cells, the changes in cell proliferation, migration, and invasion following transfection with a SNHG15 knockdown plasmid (sh-SNHG15), a miR-30b-3p inhibitor, or their co-transfection were assessed with EdU, wound healing, and Transwell assays. Bioinformatics analyses were used to predict the regulatory relationship between lncRNA SNHG15 and COX6B1, and the results were verified using Western blotting and rescue experiments in A549 cells transfected with sh-SNHG15, a COX6B1-overexpressing plasmid, or both. RESULTS: LncRNA SNHG15 was shown to target miR-30b-3p, and the former was highly expressed in lung adenocarcinoma, and associated with a poor patient prognosis. LncRNA SNHG15 was localized in the cytoplasm and expressed at higher levels in A549 and NCI-H1299 cells than in BEAS-2B cells. In A549 cells, lncRNA SNHG15 knockdown significantly inhibited cell migration, invasion and proliferation, and these changes were reversed by miR-30b-3p inhibitor. A regulatory relationship was found between lncRNA SNHG15 and COX6B1, and their expression levels were positively correlated (r=0.128, P=0.003). MiR-30b-3p knockdown obviously decreased COX6B1 expression in A549 cells, and COX6B1 overexpression rescued the cells from the inhibitory effects of lncRNA-SNHG15 knockdown. CONCLUSIONS LncRNA SNHG15 may compete with COX6B1 to bind miR-30b-3p through a ceRNA mechanism to affect proliferation, migration, and invasion of lung adenocarcinoma cells.
Humans ; MicroRNAs/metabolism* ; RNA, Long Noncoding/genetics* ; Cell Proliferation ; Cell Movement ; Lung Neoplasms/genetics* ; Adenocarcinoma of Lung ; Neoplasm Invasiveness ; A549 Cells ; Adenocarcinoma/genetics* ; Gene Expression Regulation, Neoplastic ; Cell Line, Tumor