Trichotillomania, also known as Hair Pulling Disorder, is a unique obsessive-compulsive spectrum disorder characterized by repeated removal of hair from various parts of the body. Patients attempt to control this behavior but often fail, causing impairment to important functional areas such as social interaction, work, and academics. Trichotillomania typically begins in childhood or adolescence, and is often comorbid with anxiety and depression. The resulting physical damage and changes in appearance further exacerbate the social functional impairment of patients, resulting in most patients being diagnosed only in adulthood, and missing the optimal intervention period. Current pharmacological treatments for Trichotillomania are not satisfactory, while various psychological therapies have shown potential value and prospects. Therefore, this article focuses on Trichotillomania in children and adolescents, providing a comprehensive review from multiple aspects including disease diagnosis, clinical characteristics and typing, functional impairment, neuroimaging mechanisms, and the latest developments in psychological therapy, to provide references for the clinical diagnosis, assessment, and effective intervention of Trichotillomania.

Trichotillomania, also known as Hair Pulling Disorder, is a unique obsessive-compulsive spectrum disorder characterized by repeated removal of hair from various parts of the body. Patients attempt to control this behavior but often fail, causing impairment to important functional areas such as social interaction, work, and academics. Trichotillomania typically begins in childhood or adolescence, and is often comorbid with anxiety and depression. The resulting physical damage and changes in appearance further exacerbate the social functional impairment of patients, resulting in most patients being diagnosed only in adulthood, and missing the optimal intervention period. Current pharmacological treatments for Trichotillomania are not satisfactory, while various psychological therapies have shown potential value and prospects. Therefore, this article focuses on Trichotillomania in children and adolescents, providing a comprehensive review from multiple aspects including disease diagnosis, clinical characteristics and typing, functional impairment, neuroimaging mechanisms, and the latest developments in psychological therapy, to provide references for the clinical diagnosis, assessment, and effective intervention of Trichotillomania.

Objective:To investigate clinical characteristics of and genetic variants in the NF1 gene in children with neurofibromatosis type 1 (NF1) .Methods:Clinical data were collected from 22 children with NF1, who were admitted to the Department of Dermatology, Children's Hospital, Capital Institute of Pediatrics from January 2022 to September 2023, and were analyzed. Next-generation sequencing was performed to detect NF1 mutations in the probands, and the variants were verified in the family members by Sanger sequencing. A homology modeling software was used to predict the three-dimensional protein structure, and analyze the characteristics of gene mutations.Results:Among the 22 children with NF1, there were 14 males and 8 females, and they were aged from 3 months to 12 years at the clinic visit. All the 22 children presented with multiple café-au-lait spots, and their age at onset ranged from birth to 2 years. Nine patients were accompanied by freckles in the axillary or inguinal regions, 2 by cutaneous neurofibromas, 2 by juvenile xanthogranuloma, 2 by learning disabilities, and Lisch nodules of the iris, central precocious puberty and scoliosis occurred in 1 case each; 5 cases showed characteristic manifestations of neurofibroma on brain magnetic resonance imaging. A total of 5 types of NF1 gene variants were identified in the 22 patients, including complete heterozygous deletion of the NF1 gene (1 patient), missense variants (4 patients, one of whom carried 2 types of missense variants), frameshift variants (8 patients), nonsense variants (6 patients), and classical splicing variants (3 patients). Among the 22 variants, 7 were unreported variants, including c.758T>A (p.Val253Glu), c.2360dupC (p.Thr788Asnfs*5), c.5513T>G (p.Leu1838*), c.2774dupT (p.Leu925Phefs*11), c.6894dupT (p.Val2299Cysfs*7), c.6882_6883delCT (p.Phe2295Leufs*10), and c.6448A>T (p.Lys2150*). Of the unreported variants, 6 were frameshift or nonsense variants leading to different degrees of truncated protein expression, and severely affecting protein function; based on the three-dimensional protein structure prediction analysis, it was uncertain if the missense variant c.758T>A (p.Val253Glu) affected protein conformation. In 2 children, the NF1 variants were inherited from their mothers; 1 child carried 2 NF1 missense variants, 1 of which was a spontaneous mutation potentially causing the disease, while the other one with unknown pathogenicity was inherited from the phenotypically normal father; the remaining 19 children all carried spontaneous mutations.Conclusions:Children with NF1 mainly present with multiple café-au-lait spots at the early stage, and some characteristic manifestations such as cutaneous neurofibroma, juvenile xanthogranuloma, and Lisch nodules of the iris can also occur. NF1 gene pathogenic variants are complex and diverse, and 22 variants were identified in this study, enriching the spectrum of NF1 gene variants.

The prevalence of metabolic syndrome(MetS) in patients with major depressive disorder (MDD) is significantly higher than that in healthy people. Metabolic disorder has been proven to be closely related to the onset of MDD, adverse treatment outcome and disease recurrence. Therefore, revealing the comorbidity mechanism of both is of great significance for treating MDD. Previous studies have focused on the role of abnormal cortisol levels mediated by hypothalamic-pituitary-adrenal axis disorder, but how this pathway is activated and regulated is still unclear. In recent years, with further research development, systemic inflammation induced by an abnormal immune system is considered the deep molecular mechanism of MetS comorbidity of MDD. This review aims to summarize the similar activation of innate immunity, adaptive immunity and immune signaling pathway between MDD and MetS and to provide a strong theoretical basis for follow-up mechanism exploration, drug research and intervention strategy search.

Objective To evaluate and compare the maturity of autografts and allografts as well as the postoperative clinical outcomes 10 years after anterior cruciate ligament reconstruction(ACLR).Methods A retrospective analysis was conducted on 64 patients who underwent anterior cruciate liga-ment reconstruction,with an average follow-up period of about 10 years.Autografts were used in 36 cases(56.2%),and allografts in 28 cases(43.8%).Both groups were recorded the knee Lysholm scores,IKDC subjective scores,and stability tests results(KT-1000 side-to-side difference and Lach-man test).Moreover,graft maturity was assessed using the knee magnetic resonance imaging(MRI),and the Signal-to-Noise Quotient(SNQ)for both types of grafts was measured.Results No significant differences were observed between the autograft and allograft groups in the average follow-up time(10.1±2.1 and 10.5±1.8 years)(P=0.376),the SNQ value(24.1±8.8 and 23.2±8.7)(P= 0.652),the Lysholm score(90±10.3 and 89.4±8.9)(P=0.805)and the anterior joint stability dur-ing follow-up(P=0.923).Moreover,the average IKDC score and incidence of abnormal tension of the ligament measured by KT1000 of the autograft group were higher than the allograft group[(84.5±8.3)vs.(80.4±7.8),P=0.075;14.3%vs.8.3%,P=0.724].Meanwhile,ACL re-tear occurred to two cas-es in the autograft group(5.6%)and the allograft group(7.1%),respectively,showing no significant dif-ference(P=0.795).Conclusion Ten years after ACLR,no significant differences are found in graft ma-turity,clinical outcomes,or joint stability between patients using autografts and allografts.Moreover,the rate of graft re-tear is comparable between the two groups.

Autism spectrum disorder（ASD）is a neurodevelopmental disorder with unknown etiology，and the prevalence of ASD is on the rise worldwide.Studies have found that patients with ASD have abnormal cognitive function，and objective cognitive detection tools can provide an effective method to explore the functional defects of patients with ASD.Event-related potential（ERP），which can reflect the nerve electrophysiological change in the cognitive processing of the brain，have been widely applied in the study of ASD patients in recent years due to its high temporal resolution advantage，showing a great application prospect.This article reviews the clinical application of ERP in children with ASD，in order to reveal the functional defects of ASD children from the perspective of nerve electrophysiology，and provide a reference for the assessment and even early screening of ASD.

Autism spectrum disorder（ASD）is a serious neurodevelopmental disorder，with deficits in social and language communication，rigid behaviors，limited interests and activities. At present，research on the pathogenesis of ASD involving immunity has been making progress worldwide. In terms of cytokines（such as IL-1β，IL-8，IL-17，etc.）and ASD animal models，it has been found that the onset of ASD is associated with nervous system immune dysfunction，which may lead to synaptic function impairment. The purpose of this review is to describe the recent research on ASD and immune dysfunction to provide ideas for exploring the etiology，pathogenesis and potential therapeutic measures of ASD.

Objective:To analyze the clinical and immunological characteristics of children with acute viral infection-related encephalopathy.Methods:Case-control study.A retrospective analysis was conducted on the clinical data of children diagnosed with acute viral infection-related encephalopathy during hospitalization at the Children′s Hospital, Capital Institute of Pediatrics from January 2020 to January 2023.According to the last follow-up modified Rankin scale (mRS) score, these children were divided into a good prognosis group (mRS score ≤2) and a poor prognosis group (mRS score >2), and the clinical and immunological characteristics of the children with different prognoses were analyzed.The binary Logistic regression was used to analyze the risk factors for poor prognosis.Results:A total of 28 children with acute viral infection-related encephalopathy aged 4 months to 11 years were included.There were 16 males (57%) and 12 females (43%). Among the preinfection viruses, there were 16 children of Corona virus disease 2019, 8 children of influenza A virus, 3 children of influenza B virus, and 1 child of norovirus.Among them, there were 21 children with acute necrotizing encephalopathy, 4 children with acute encephalopathy with biphasic seizures and late reduced diffusion, 2 children with mild encephalitis with a reversible splenial lesion, and 1 child with hemorrhagic shock and encephalopathy syndrome.Among the first symptoms, 24 children (85.7%) had consciousness disorders, 23 children (82.1%) had seizures, 17 children (60.7%) had speech disorders, 11 children (39.3%) had involuntary movements, and 10 children (35.7%) had abnormal mental behavior.For the site of lesion, the cranial nuclear magnetic resonance imaging revealed 17 in the thalamus, 10 in the brainstem, 9 in the basal ganglia, 8 in the cerebellar hemisphere, and 4 in the corpus callosum.In the last follow-up evaluation, 17 children had a mRS score of >2, and 11 children had a mRS score of ≤2.Univariate analysis showed that disturbance of consciousness, seizure cluster, brain stem lesion, absolute value of serum T lymphocytes, cerebrospinal fluid(CSF) protein, CSF cytokines [interleukin(IL)-1β, IL-6 and IL-8]were higher in the poor prognosis group than those in the good prognosis group.Multivariate Logistic regression analysis indicated that brain stem disease, CSF IL-1β and T lymphocyte absolute number were independent risk factors for poor prognosis.Conclusions:Brain stem lesions, cerebrospinal fluid IL-1β and the absolute number of T lymphocytes have predictive value for the prognosis of acute viral infection-associated encephalopathy.The more severe the conditions, the lower the T lymphocytes, and the higher the cytokines in some cerebrospinal fluid.

The prevalence of metabolic syndrome(MetS) in patients with major depressive disorder (MDD) is significantly higher than that in healthy people. Metabolic disorder has been proven to be closely related to the onset of MDD, adverse treatment outcome and disease recurrence. Therefore, revealing the comorbidity mechanism of both is of great significance for treating MDD. Previous studies have focused on the role of abnormal cortisol levels mediated by hypothalamic-pituitary-adrenal axis disorder, but how this pathway is activated and regulated is still unclear. In recent years, with further research development, systemic inflammation induced by an abnormal immune system is considered the deep molecular mechanism of MetS comorbidity of MDD. This review aims to summarize the similar activation of innate immunity, adaptive immunity and immune signaling pathway between MDD and MetS and to provide a strong theoretical basis for follow-up mechanism exploration, drug research and intervention strategy search.

Mood disorders are a group of mental conditions characterized by significant and lasting mood or emotional changes, which seriously affect patients′ normal lives. However, the pathogenesis of mood disorders is still unclear, and the specific biological markers to assist the diagnosis are still not determined, and this affects the diagnosis, treatment and prognosis. With the development of molecular imaging, positron emission tomography (PET) has been widely used in clinical research on mood disorders, which is helpful for their clinical diagnosis and treatment. This paper aims to review the research progress on PET imaging principles, the pathogenesis and treatment mechanism of mood disorders, and to summarize the application prospect of PET in mood disorders.