COVID-19 vaccinations for patients with epilepsy in Guizhou Province, China: A cross-sectional study.

Several COVID-19 vaccines have been approved for emergency use according to China's immunization programs. These vaccines has created hope for patients with epilepsy, because the vaccines can help to reduce their risk of becoming infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The aim of this study was to investigate the COVID-19 vaccine safety in patients with epilepsy. Here, we assessed the time of symptom control and the features of adverse events of seizure patients following their COVID-19 vaccinations. The results showed that adverse events of COVID-19 vaccinations for epilepsy patients included local pain at the injection site, dizziness and headache, epileptic attack, somnolence, limb weakness, limb pain, allergy, and fever. In addition, the average recovery time of the adverse events was approximately 42 h. More importantly, our study showed that it was relatively safe to vaccinate epilepsy patients who did not experience seizures for approximately 12 months prior to the immunization date.

Invasive pneumococcal diseases in Chinese children: a multicentre hospital-based active surveillance from 2019 to 2021.

This study aimed to provide data for the clinical features of invasive pneumococcal disease (IPD) and the molecular characteristics of Streptococcus pneumoniae isolates from paediatric patients in China. We conducted a multi-centre prospective study for IPD in 19 hospitals across China from January 2019 to December 2021. Data of demographic characteristics, risk factors for IPD, death, and disability was collected and analysed. Serotypes, antibiotic susceptibility, and multi-locus sequence typing (MLST) of pneumococcal isolates were also detected. A total of 478 IPD cases and 355 pneumococcal isolates were enrolled. Among the patients, 260 were male, and the median age was 35 months (interquartile range, 12-46 months). Septicaemia (37.7%), meningitis (32.4%), and pneumonia (27.8%) were common disease types, and 46 (9.6%) patients died from IPD. Thirty-four serotypes were detected, 19F (24.2%), 14 (17.7%), 23F (14.9%), 6B (10.4%) and 19A (9.6%) were common serotypes. Pneumococcal isolates were highly resistant to macrolides (98.3%), tetracycline (94.1%), and trimethoprim/sulfamethoxazole (70.7%). Non-sensitive rates of penicillin were 6.2% and 83.3% in non-meningitis and meningitis isolates. 19F-ST271, 19A-ST320 and 14-ST876 showed high resistance to antibiotics. This multi-centre study reports the clinical features of IPD and demonstrates serotype distribution and antibiotic resistance of pneumococcal isolates in Chinese children. There exists the potential to reduce IPD by improved uptake of pneumococcal vaccination, and continued surveillance is warranted.

Retracted: Expression of TP53, BCL-2, and VEGFA Genes in Esophagus Carcinoma and its Biological Significance.

The Editors of Medical Science Monitor wish to inform you that the above manuscript has been retracted from publication due to concerns with the credibility and originality of the study, the manuscript content, and the Figure images. Reference: Wei Wei, Yanqin Wang, Xiaoming Yu, Lan Ye, Yuhua Jiang, Yufeng Cheng. Expression of TP53, BCL-2, and VEGFA Genes in Esophagus Carcinoma and its Biological Significance. Med Sci Monit, 2015; 21: 3016-3022. DOI: 10.12659/MSM.894640.

A Workflow for Meaningful Interpretation of Classification Results from Handheld Ambient Mass Spectrometry Analysis Probes.

While untargeted analysis of biological tissues with ambient mass spectrometry analysis probes has been widely reported in the literature, there are currently no guidelines to standardize the workflows for the experimental design, creation, and validation of molecular models that are utilized in these methods to perform class predictions. By drawing parallels with hurdles that are faced in the field of food fraud detection with untargeted mass spectrometry, we provide a stepwise workflow for the creation, refinement, evaluation, and assessment of the robustness of molecular models, aimed at meaningful interpretation of mass spectrometry-based tissue classification results. We propose strategies to obtain a sufficient number of samples for the creation of molecular models and discuss the potential overfitting of data, emphasizing both the need for model validation using an independent cohort of test samples, as well as the use of a fully characterized feature-based approach that verifies the biological relevance of the features that are used to avoid false discoveries. We additionally highlight the need to treat molecular models as "dynamic" and "living" entities and to further refine them as new knowledge concerning disease pathways and classifier feature noise becomes apparent in large(r) population studies. Where appropriate, we have provided a discussion of the challenges that we faced in our development of a 10 s cancer classification method using picosecond infrared laser mass spectrometry (PIRL-MS) to facilitate clinical decision-making at the bedside.

HDAC3 promotes Sertoli cell maturation and maintains the blood-testis barrier dynamics.

Germ cell development depends on the capacity of somatic Sertoli cells to undergo differentiation into a mature state and establish a germ cell-specific blood-testis barrier (BTB). The BTB structure confers an immunological barrier for meiotic and postmeiotic germ cells, and its dynamic permeability facilitates a transient movement of preleptotene spermatocytes through BTB to enter meiosis. However, the regulatory factors involved in Sertoli cell maturation and how BTB dynamics coordinate germ cell development remain unclear. Here, we found a histone deacetylase HDAC3 abundantly expresses in Sertoli cells and localizes in both cytoplasm and nucleus. Sertoli cell-specific Hdac3 knockout in mice causes infertility with compromised integrity of blood-testis barrier, leading to germ cells unable to traverse through BTB and an accumulation of preleptotene spermatocytes in juvenile testis. Mechanistically, nuclear HDAC3 regulates the expression program of Sertoli cell maturation genes, and cytoplasmic HDAC3 forms a complex with the gap junction protein Connexin 43 to modulate the BTB integrity and dynamics through regulating the distribution of tight junction proteins. Our findings identify HDAC3 as a critical regulator in promoting Sertoli cell maturation and maintaining the homeostasis of the blood-testis barrier.

The comorbidity profiles and medication issues of patients with multiple system atrophy: a systematic cross-sectional analysis.

BACKGROUND: Multiple system atrophy (MSA) is a complex and fatal neurodegenerative movement disorder. Understanding the comorbidities and drug therapy is crucial for MSA patients' safety and management. OBJECTIVES: To investigate the pattern of comorbidities and aspects of drug therapy in MSA patients. METHODS: Cross-sectional data of MSA patients according to Gilman et al. (2008) diagnostic criteria and control patients without neurodegenerative diseases (non-ND) were collected from German, multicenter cohorts. The prevalence of comorbidities according to WHO ICD-10 classification and drugs administered according to WHO ATC system were analyzed. Potential drug-drug interactions were identified using AiDKlinik®. RESULTS: The analysis included 254 MSA and 363 age- and sex-matched non-ND control patients. MSA patients exhibited a significantly higher burden of comorbidities, in particular diseases of the genitourinary system. Also, more medications were prescribed MSA patients, resulting in a higher prevalence of polypharmacy. Importantly, the risk of potential drug-drug interactions, including severe interactions and contraindicated combinations, was elevated in MSA patients. When comparing MSA-P and MSA-C subtypes, MSA-P patients suffered more frequently from diseases of the genitourinary system and diseases of the musculoskeletal system and connective tissue. CONCLUSIONS: MSA patients face a substantial burden of comorbidities, notably in the genitourinary system. This, coupled with increased polypharmacy and potential drug interactions, highlights the complexity of managing MSA patients. Clinicians should carefully consider these factors when devising treatment strategies for MSA patients.

Stabilization of MOF (KAT8) by USP10 promotes esophageal squamous cell carcinoma proliferation and metastasis through epigenetic activation of ANXA2/Wnt signaling.

Dysregulation of MOF (also known as MYST1, KAT8), a highly conserved H4K16 acetyltransferase, plays important roles in human cancers. However, its expression and function in esophageal squamous cell carcinoma (ESCC) remain unknown. Here, we report that MOF is highly expressed in ESCC tumors and predicts a worse prognosis. Depletion of MOF in ESCC significantly impedes tumor growth and metastasis both in vitro and in vivo, whereas ectopic expression of MOF but not catalytically inactive mutant (MOF-E350Q) promotes ESCC progression, suggesting that MOF acetyltransferase activity is crucial for its oncogenic activity. Further analysis reveals that USP10, a deubiquitinase highly expressed in ESCC, binds to and deubiquitinates MOF at lysine 410, which protects it from proteosome-dependent protein degradation. MOF stabilization by USP10 promotes H4K16ac enrichment in the ANXA2 promoter to stimulate ANXA2 transcription in a JUN-dependent manner, which subsequently activates Wnt/ß-Catenin signaling to facilitate ESCC progression. Our findings highlight a novel USP10/MOF/ANXA2 axis as a promising therapeutic target for ESCC.

scSID: A lightweight algorithm for identifying rare cell types by capturing differential expression from single-cell sequencing data.

Single-cell RNA sequencing (scRNA-seq) is currently an important technology for identifying cell types and studying diseases at the genetic level. Identifying rare cell types is biologically important as one of the downstream data analyses of single-cell RNA sequencing. Although rare cell identification methods have been developed, most of these suffer from insufficient mining of intercellular similarities, low scalability, and being time-consuming. In this paper, we propose a single-cell similarity division algorithm (scSID) for identifying rare cells. It takes cell-to-cell similarity into consideration by analyzing both inter-cluster and intra-cluster similarities, and discovers rare cell types based on the similarity differences. We show that scSID outperforms other existing methods by benchmarking it on different experimental datasets. Application of scSID to multiple datasets, including 68K PBMC and intestine, highlights its exceptional scalability and remarkable ability to identify rare cell populations.

The Emerging Therapeutic Role of Prostaglandin E2 Signaling in Pulmonary Hypertension.

Mild-to-moderate pulmonary hypertension (PH) is a common complication of chronic obstructive pulmonary disease (COPD). It is characterized by narrowing and thickening of the pulmonary arteries, resulting in increased pulmonary vascular resistance (PVR) and ultimately leading to right ventricular dysfunction. Pulmonary vascular remodeling in COPD is the main reason for the increase of pulmonary artery pressure (PAP). The pathogenesis of PH in COPD is complex and multifactorial, involving chronic inflammation, hypoxia, and oxidative stress. To date, prostacyclin and its analogues are widely used to prevent PH progression in clinical. These drugs have potent anti-proliferative, anti-inflammatory, and stimulating endothelial regeneration properties, bringing therapeutic benefits to the slowing, stabilization, and even some reversal of vascular remodeling. As another well-known and extensively researched prostaglandins, prostaglandin E2 (PGE2) and its downstream signaling have been found to play an important role in various biological processes. Emerging evidence has revealed that PGE2 and its receptors (i.e., EP1-4) are involved in the regulation of pulmonary vascular homeostasis and remodeling. This review focuses on the research progress of the PGE2 signaling pathway in PH and discusses the possibility of treating PH based on the PGE2 signaling pathway.

Signaling pathways in hair aging.

Hair follicle (HF) homeostasis is regulated by various signaling pathways. Disruption of such homeostasis leads to HF disorders, such as alopecia, pigment loss, and hair aging, which is causing severe health problems and aesthetic concerns. Among these disorders, hair aging is characterized by hair graying, hair loss, hair follicle miniaturization (HFM), and structural changes to the hair shaft. Hair aging occurs under physiological conditions, while premature hair aging is often associated with certain pathological conditions. Numerous investigations have been made to determine the mechanisms and explore treatments to prevent hair aging. The most well-known hypotheses about hair aging include oxidative stress, hormonal disorders, inflammation, as well as DNA damage and repair defects. Ultimately, these factors pose threats to HF cells, especially stem cells such as hair follicle stem cells, melanocyte stem cells, and mesenchymal stem cells, which hamper hair regeneration and pigmentation. Here, we summarize previous studies investigating the above mechanisms and the existing therapeutic methods for hair aging. We also provide insights into hair aging research and discuss the limitations and outlook.

Downregulation of NHE1 expression attenuates apoptosis of primary hippocampal neurons of an epilepsy model through the calpain-1 pathway.

OBJECTIVE: Na(+)/H(+) exchanger isoform 1 (NHE1), a membrane protein that regulates intracellular pH, is abundantly expressed in brain tissues. It is associated with pathophysiologies in several brain diseases. The present study aimed to investigate the effects of NHE1 on the apoptosis of primary neurons of an epilepsy model. METHODS: Primary hippocampal neurons were cultured in an Mg2+-free medium to establish an epilepsy cell model. Designed shNHE1 lentivirus was used to silence NHE1 level in primary neurons. Nonselective pharmacological inhibitor MDL-28170 (20 µmol/L) was used to inhibit calpain-1 protein in neurons treated with Mg2+-free medium. The expression levels of NHE1 and calpain-1, intracellular Ca2+ (Ca2+i) and H+ (H+i) levels, and the expression levels of apoptosis-related proteins Bcl-2 and Bax were detected in neurons. TUNEL staining was performed to determine apoptosis in different groups. RESULTS: NHE1 expression was increased in primary neurons treated with an Mg2+-free medium, and it was correlated with increased expression of calpain-1 and cell apoptosis. Neurons from the in vitro epilepsy model showed significantly decreased Bcl-2 protein expression and significantly increased Bax protein expression. In the presence of LV-shNHE1 and the calpain-1 inhibitor MDL-28170, the changes in the expression of apoptosis-related proteins Bcl-2 and Bax were blocked in the epileptic model, and the percentage of apoptotic neurons among neurons from the in vitro epilepsy model was significantly decreased. The increase in calpain-1 expression was suppressed by LV-shNHE1; however, the inhibition of calpain-1 did not affect NHE1 expression. CONCLUSION: These results demonstrate that NHE1 participates in the promotion of neuronal apoptosis of epilepsy model in vitro through the calpain-1 pathway. Downregulation of NHE1 expression could exert a neuroprotective effect on epilepsy.

Metabolic Lipids in Melanoma Enable Rapid Determination of Actionable BRAF-V600E Mutation with Picosecond Infrared Laser Mass Spectrometry in 10 s.

Rapid molecular profiling of biological tissues with picosecond infrared laser mass spectrometry (PIRL-MS) has enabled the detection of clinically important histologic types and molecular subtypes of human cancers in as little as 10 s of data collection and analysis time. Utilizing an engineered cell line model of actionable BRAF-V600E mutation, we observed statistically significant differences in 10 s PIRL-MS molecular profiles between BRAF-V600E and BRAF-wt cells. Multivariate statistical analyses revealed a list of mass-to-charge (m/z) values most significantly responsible for the identification of BRAF-V600E mutation status in this engineered cell line that provided a highly controlled testbed for this observation. These metabolites predicted BRAF-V600E expression in human melanoma cell lines with greater than 98% accuracy. Through chromatography and tandem mass spectrometry analysis of cell line extracts, a 30-member "metabolite array" was characterized for determination of BRAF-V600E expression levels in subcutaneous melanoma xenografts with an average sensitivity and specificity of 95.6% with 10 s PIRL-MS analysis. This proof-of-principle work warrants a future large-scale study to identify a metabolite array for 10 s determination of actionable BRAF-V600E mutation in human tissue to guide patient care.

Downregulating NHE-1 decreases the apoptosis of hippocampal cells in epileptic model rats based on the NHE-1/calpain1 pathway.

Seizure is associated with pathological changes of hippocampus, but the mechanism by which hippocampal neuronal apoptosis promotes epilepsy is unclear. Our previous study showed that the expression of NHE-1 was increased in epileptic model rats. Therefore, this study further explores the effect of NHE-1 on hippocampal cells apoptosis and seizure in lithium chloride-pilocarpine epileptic model rats. First, we established a lithium chloride-pilocarpine induced epileptic rat model and detected the expression of NHE-1, calpain1 and apoptosis in the hippocampus. Then, we further down-regulated NHE-1 to observe the expression of calpain1 and apoptosis in the hippocampus, as well as its effect on seizures in rats. We found that the expression of NHE-1 and calpain1 and apoptosis in the hippocampus was significant increased in the model group. After down-regulating NHE-1, the expression of calpain1 was decreased, and hippocampal cell apoptosis was alleviated. In addition, down-regulation of NHE-1 reduced the frequency and duration of seizures in epileptic rats. Therefore, hippocampal NHE-1 overexpression is closely related to the development of neuronal apoptosis in a rat model of epilepsy, and downregulating NHE-1 expression can reduce cell apoptosis. Moreover, the NHE-1/calpain1 signaling pathway may be an important mechanism leading to hippocampal cell apoptosis.

The molecular mechanism of WRINKLED1 transcription factor regulating oil accumulation in developing seeds of castor bean.

The transcription factor WRINKLED1 (WRI1), a member of AP2 gene family that contain typical AP2 domains, has been considered as a master regulator regulating oil biosynthesis in oilseeds. However, the regulatory mechanism of RcWRI1 in regulating oil accumulation during seed development has not been clearly addressed. Castor bean (Ricinus communis) is one of the most important non-edible oil crops and its seed oils are rich in hydroxy fatty acids, widely applied in industry. In this study, based on castor bean reference genome, three RcWRIs genes (RcWRI1, RcWRI2 and RcWRI3) were identified and the expressed association of RcWRI1 with oil accumulation were determined. Heterologous transformation of RcWRI1 significantly increased oil content in tobacco leaf, confirming that RcWRI1 activate lipid biosynthesis pathway. Using DNA Affinity Purification sequencing (DAP-seq) technology, we confirmed RcWRI1 binding with Transcription Start Site of genes and identified 7961 WRI1-binding candidate genes. Functionally, these identified genes were mainly involved in diverse metabolism pathways (including lipid biosynthesis). Three cis-elements AW-box ([CnTnG](n)7[CG]) and AW-boxes like ([GnAnC](n)6[GC]/[GnAnC](n)7[G]) bound with RcWRI1 were identified. Co-expression network analysis of RcWRI1 further found that RcWRI1 might be widely involved in biosynthesis of storage materials during seed development. In particular, yeast one hybrid experiments found that both AP2 domains within RcWRI1 were required in binding targeted genes. These results not only provide new evidence to understand the regulatory mechanism of RcWRI1 in regulation of oil accumulation during castor bean seed development, but also give candidate gene resource for subsequent genetic improvement toward increasing oil content in oilseed crops.

[Advances in the electrophysiological research on neurocognitive function in adolescents with non-suicidal self-injury]. / éžè‡ªæ€æ€§è‡ªä¼¤é’å°‘å¹´ç¥žç»è®¤çŸ¥åŠŸèƒ½ç›¸å ³ç”µç”Ÿç†ç ”ç©¶è¿›å±•.

Non-suicidal self-injury (NSSI) is becoming increasingly common in adolescents and seriously affects their physical and mental health, and it is also a major risk factor for suicide among adolescents. NSSI has now become a public health issue of general concern; however, the identification of cognitive dysfunction in NSSI is still based on neuropsychological cognitive assessment and subjective questionnaire assessment, with a lack of objective evaluation indicators. As a method for studying the cognitive neural mechanism of NSSI, electroencephalography is a reliable tool for finding objective biomarkers of NSSI. This article reviews the recent research on electrophysiology associated with cognitive dysfunction in adolescents with NSSI.

scASGC: An adaptive simplified graph convolution model for clustering single-cell RNA-seq data.

Single-cell RNA sequencing (scRNA-seq) is now a successful technique for identifying cellular heterogeneity, revealing novel cell subpopulations, and forecasting developmental trajectories. A crucial component of the processing of scRNA-seq data is the precise identification of cell subpopulations. Although many unsupervised clustering methods have been developed to cluster cell subpopulations, the performance of these methods is vulnerable to dropouts and high dimensionality. In addition, most existing methods are time-consuming and fail to adequately account for potential associations between cells. In the manuscript, we present an unsupervised clustering method based on an adaptive simplified graph convolution model called scASGC. The proposed method builds plausible cell graphs, aggregates neighbor information using a simplified graph convolution model, and adaptively determines the most optimal number of convolution layers for various graphs. Experiments on 12 public datasets show that scASGC outperforms both classical and state-of-the-art clustering methods. In addition, in a study of mouse intestinal muscle containing 15,983 cells, we identified distinct marker genes based on the clustering results of scASGC. The source code of scASGC is available at https://github.com/ZzzOctopus/scASGC.

Alpha lipoic acid ameliorates motor deficits by inhibiting ferroptosis in Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disease. Ferroptosis shares several features with PD pathophysiology, and anti-ferroptosis molecules are neuroprotective in PD animal models. As an antioxidant and iron chelating agent, alpha lipoic acid (ALA) has a neuroprotective effect on PD; however, the influence of ALA on ferroptosis in PD remains unclear. This study aimed to determine the mechanism of ALA in regulating ferroptosis in PD models. Results showed that ALA could ameliorate motor deficits in PD models and regulate iron metabolism by upregulating ferroportin (FPN) and ferritin heavy chain 1 (FTH1) and downregulating iron importer divalent metal transporter 1 (DMT1). Moreover, ALA decreased the accumulation of reactive oxygen species (ROS) and lipid peroxidation, rescued mitochondrial damage, and prevented ferroptosis effectively by inhibiting the downregulation of glutathione peroxidase 4 (GPX4) and cysteine/glutamate transporter (xCT) in PD. Mechanistic study indicated that the activation of SIRT1/NRF2 pathway was involved in the upregulation effect of GPX4 and FTH1. Thus, ALA ameliorates motor deficits in PD models by regulating iron metabolism and mitigating ferroptosis through the SIRT1/NRF2 signaling pathway.

High carrier frequency of pathogenic PATL2 gene mutations predicted in population: a bioinformatics-based approach.

Topoisomerase II homologue 2 (PATL2) has been confirmed to be a key gene that contributes to oocyte maturation. However, the allele distribution and carrier frequency of these mutations remain uncharacterized. So a bioinformatics subcategory analysis of PATL2 mutations from outcome data and Single Nucleotide Polymorphism (SNP) databases was conducted. Altogether, the causative PATL2 mutation number detected in patients with oocyte maturation defects in the clinical studies and pathogenic PATL2 mutation sites predicted by software based on the database was approximately 53. The estimated carrier frequency of pathogenic mutation sites was at least 1.14‰ based on the gnomAD and ExAC database, which was approximately 1/877. The highest frequency of mutations detected in the independent patients was c.223-14_223-2del13. The carrier frequency of this mutation in the population was 0.25‰, which may be a potential threat to fertility. Estimated allele and carrier frequency are relatively higher than those predicted previously based on clinical ascertainment. A review of PATL2 mutation lineage identified in 34 patients showed that 53.81%, 9.22% and 14.72% of the oocytes with PATL2 mutations were arrested at the germinal vesicle (GV) stage, metaphase I (MI) stage and first polar body stage, respectively. Oocytes that could develop to the first polar body stage were extremely rare to fertilise, and their ultimate fate was early embryonic arrest. Phenotypic variability is related to the function of the regions and degree of loss of function of PATL2 protein. A 3D protein structure changes predicted by online tools, AlphaFold, showed aberrations at the mutation sites, which may explain partially the function loss. When the mutated and wild-type proteins are not in the same amino acid category, the protein structure will be considerably unstable. The integration of additional mutation sites with phenotypes is helpful in drawing a complete picture of the disease. Bioinformatics analysis of PATL2 mutations will help reveal molecular epidemiological characteristics and provide an important reference for new mutation assessment, genetic counselling and drug research.

Single-cell RNA-seq uncovers dynamic processes orchestrated by RNA-binding protein DDX43 in chromatin remodeling during spermiogenesis.

Mammalian spermatogenesis shows prominent chromatin and transcriptomic switches in germ cells, but it is unclear how such dynamics are controlled. Here we identify RNA helicase DDX43 as an essential regulator of the chromatin remodeling process during spermiogenesis. Testis-specific Ddx43 knockout mice show male infertility with defective histone-to-protamine replacement and post-meiotic chromatin condensation defects. The loss of its ATP hydrolysis activity by a missense mutation replicates the infertility phenotype in global Ddx43 knockout mice. Single-cell RNA sequencing analyses of germ cells depleted of Ddx43 or expressing the Ddx43 ATPase-dead mutant reveals that DDX43 regulates dynamic RNA regulatory processes that underlie spermatid chromatin remodeling and differentiation. Transcriptomic profiling focusing on early-stage spermatids combined with enhanced crosslinking immunoprecipitation and sequencing further identifies Elfn2 as DDX43-targeted hub gene. These findings illustrate an essential role for DDX43 in spermiogenesis and highlight the single-cell-based strategy to dissect cell-state-specific regulation of male germline development.

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Biogenetics plays an important role in the pathogenesis of depressive disorder in adolescents. Various genetic polymorphism studies have updated the understanding of adolescent depressive disorder. However, due to the influence of gene-environment interaction and age of puberty, the influence of gene polymorphisms on adolescent depressive disorder is complicated to clarify. Investigating and clarifying the relationship between gene polymorphisms and adolescent depressive disorder will promote the research on the pathogenesis of this disorder and provide a reference for the prevention and treatment of this disorder. This article reviews the genetic polymorphisms related to adolescent depressive disorder.