Rbm24 controls poly(A) tail length and translation efficiency of crystallin mRNAs in the lens via cytoplasmic polyadenylation.

Lens transparency is established by abundant accumulation of crystallin proteins and loss of organelles in the fiber cells. It requires an efficient translation of lens messenger RNAs (mRNAs) to overcome the progressively reduced transcriptional activity that results from denucleation. Inappropriate regulation of this process impairs lens differentiation and causes cataract formation. However, the regulatory mechanism promoting protein synthesis from lens-expressed mRNAs remains unclear. Here we show that in zebrafish, the RNA-binding protein Rbm24 is critically required for the accumulation of crystallin proteins and terminal differentiation of lens fiber cells. In the developing lens, Rbm24 binds to a wide spectrum of lens-specific mRNAs through the RNA recognition motif and interacts with cytoplasmic polyadenylation element-binding protein (Cpeb1b) and cytoplasmic poly(A)-binding protein (Pabpc1l) through the C-terminal region. Loss of Rbm24 reduces the stability of a subset of lens mRNAs encoding heat shock proteins and shortens the poly(A) tail length of crystallin mRNAs encoding lens structural components, thereby preventing their translation into functional proteins. This severely impairs lens transparency and results in blindness. Consistent with its highly conserved expression in differentiating lens fiber cells, the findings suggest that vertebrate Rbm24 represents a key regulator of cytoplasmic polyadenylation and plays an essential role in the posttranscriptional control of lens development.

Improving the taxonomy of fossil pollen using convolutional neural networks and superresolution microscopy.

Taxonomic resolution is a major challenge in palynology, largely limiting the ecological and evolutionary interpretations possible with deep-time fossil pollen data. We present an approach for fossil pollen analysis that uses optical superresolution microscopy and machine learning to create a quantitative and higher throughput workflow for producing palynological identifications and hypotheses of biological affinity. We developed three convolutional neural network (CNN) classification models: maximum projection (MPM), multislice (MSM), and fused (FM). We trained the models on the pollen of 16 genera of the legume tribe Amherstieae, and then used these models to constrain the biological classifications of 48 fossil Striatopollis specimens from the Paleocene, Eocene, and Miocene of western Africa and northern South America. All models achieved average accuracies of 83 to 90% in the classification of the extant genera, and the majority of fossil identifications (86%) showed consensus among at least two of the three models. Our fossil identifications support the paleobiogeographic hypothesis that Amherstieae originated in Paleocene Africa and dispersed to South America during the Paleocene-Eocene Thermal Maximum (56 Ma). They also raise the possibility that at least three Amherstieae genera (Crudia, Berlinia, and Anthonotha) may have diverged earlier in the Cenozoic than predicted by molecular phylogenies.

Label-Free Detection of CA19-9 Using a BSA/Graphene-Based Antifouling Electrochemical Immunosensor.

Evaluating the levels of the biomarker carbohydrate antigen 19-9 (CA19-9) is crucial in early cancer diagnosis and prognosis assessment. In this study, an antifouling electrochemical immunosensor was developed for the label-free detection of CA19-9, in which bovine serum albumin (BSA) and graphene were cross-linked with the aid of glutaraldehyde to form a 3D conductive porous network on the surface of an electrode. The electrochemical immunosensor was characterized through the use of transmission electron microscopy (TEM), scanning electron microscopy (SEM), atomic force microscope (AFM), UV spectroscopy, and electrochemical methods. The level of CA19-9 was determined through the use of label-free electrochemical impedance spectroscopy (EIS) measurements. The electron transfer at the interface of the electrode was well preserved in human serum samples, demonstrating that this electrochemical immunosensor has excellent antifouling performance. CA19-9 could be detected in a wide range from 13.5 U/mL to 1000 U/mL, with a detection limit of 13.5 U/mL in human serum samples. This immunosensor also exhibited good selectivity and stability. The detection results of this immunosensor were further validated and compared using an enzyme-linked immunosorbent assay (ELISA). All the results confirmed that this immunosensor has a good sensing performance in terms of CA19-9, suggesting its promising application prospects in clinical applications.

A Rare Case of Hb H Disease and Systemic Lupus Erythematosus.

Anemia is common in patients with systemic lupus erythematosus (SLE). The association between thalassemia and SLE is rare. In this study, we report the first patient who was found to have a severe hemolytic anemia caused by combination of SLE and Hb H disease. The patient had a more severe presentation in the hematological system. Our case indicates that for a patient who was diagnosed with SLE and developed deterioration in her hematological cell lines, investigation of other possible coexisting causes would be warranted.

Different culture method changing CD105 expression in amniotic fluid MSCs without affecting differentiation ability or immune function.

MSCs are kind of cultured cells that reside in different tissues as inducers or regulators of physiological and pathological processes. Here, we derived MSCs from amniotic fluid and compared their differentiation ability and immunosuppression effect on PHA-activated PBMC with those of MSCs isolated from umbilical cords. Amniotic fluid MSCs were isolated and cultured on commercial AFC medium and classic MSC medium, and the number and size of colonies were used to evaluate differences in primary and passaged culture. Rate of proliferation, population doubling time, cell morphology, cell surface markers and mRNA expression were measured in subcultured cells. Furthermore, a comparative study was performed with umbilical cord MSCs to assess the ability of differentiation and immunosuppressive effect of PHA-stimulated PBMCs. Amniotic fluid MSCs were isolated and expanded by three methods, and exhibited nearly all the characteristics of umbilical cord MSCs. Compared with umbilical cord MSCs, amniotic fluid MSCs had an enhanced osteogenic and chrondrogenic differentiation capability, and stronger immunosuppression effect of inhibition of PHA-activated PBMC division. Culture with commercial AFCs medium yielded the highest percentage of CD105 expression and showed some advantages in primary cell isolation, cell source-specific marker retention and cell proliferation. We demonstrated that amniotic fluid MSCs exhibited some advantages over umbilical cord MSCs, and different culture media caused cell proliferation, cell surface marker and cell morphology change, but were not associated with varying differentiation capability and immune effects.

Comparison of different zinc precursors for the construction of zeolitic imidazolate framework-8 artificial shells on living cells.

The robust cell-in-shell structure is highly desirable for endowing living cells with an artificial exoskeleton to defend them from many environmental factors such as osmotic pressure, shear force, heat, UV radiation, and enzymes. Cell encapsulation has shown potential applications in many fields and attracted increasing interest. However, the influences of the precursors on the cell viability during the shell formation process are not clear and seldom investigated. Here, zinc nitrite, zinc acetate and zinc sulfate were applied individually to synthesize zeolitic imidazolate framework-8 (ZIF-8) shells on living cells. All the zinc salt precursors could convert to a ZIF-8 layer on the living cell surface. The zinc salts and organic ligand did not exhibit obvious toxicity to yeast cells when applied individually. However, dead cells were observed during the living cell encapsulation process using different zinc precursors. Compared with zinc nitrate and zinc acetate, ZIF-8 formed by zinc sulfate led to a higher percentage of cell death, especially under high concentrations of zinc sulfate. Cell division was suppressed by the ZIF-8 shell but restored fully upon shell removal by EDTA solution or pH 4.0 buffer. Escherichia coli (E. coli) cells showed a lower percentage of cell death, indicating excellent tolerance to the ZIF-8 encapsulation process. This work illustrates the cell toxicity during the formation of ZIF-8 cell shells by different zinc salts and engineering of the cell growth by MOF coating, which could provide a foundation for further quantitative analysis and potential applications in biomedicine and bioengineering.

Prevalence and risk of thyroid diseases in myasthenia gravis.

OBJECTIVES: To estimate the prevalence of thyroid diseases and the cumulative risk of thyroid diseases during a follow-up period after myasthenia gravis (MG) diagnosis compared with non-MG controls. MATERIALS AND METHODS: We used the Taiwan National Health Insurance Database linked to Registry of Catastrophic Illness database to identify patients with MG. The controls were composed of those who did not have MG and were matched with the MG patients by sex, age, and the index date. We recorded thyroid disease histories before and after the index date. RESULTS: Our study included 5813 MG patients and 29 065 controls. The prevalence of thyroid diseases in the MG patients at diagnosis was 18.4%, which was nearly 3.9-fold greater than that in the control group. (Odds ratio [OR] 3.895, 95% Confidence interval [CI] 3.574-4.246) After excluding pre-existing thyroid diseases, the incidence of comorbid thyroid diseases was 8.7% in the MG patients and 4% in the control group. The MG patients had a 2.36-fold increased risk of developing thyroid diseases compared to the control group. (crude hazard ratio [HR] 2.360, 95% CI 2.095-2.659) The cumulative probabilities of developing thyroid diseases at 1, 5, and 10 years after the index date were 21.6%, 24.9%, and 28.7%, respectively, in the MG patients, while the cumulative probabilities were 6.5%, 8.8%, and 11.8%, respectively, in control group (log-rank test <0.0001). CONCLUSIONS: The current population-based study showed a higher prevalence of pre-existing thyroid diseases and a higher cumulative probability of thyroid diseases during follow-up after MG diagnosis than in the general population.

[Evolvement of a five-way translocation t(5;9;22;6;17) from a four-way Philadelphia translocation t(5;9;22;6) in a rare case of chronic myeloid leukemia].

OBJECTIVE: To trace a rare case of chronic myeloid leukemia (CML) with a four-way Philadelphia chromosome variant by cytogenetic analysis in order to provide a basis for the selection of treatment. METHODS: Bone marrow morphology, chromosomal karyotyping, fluorescence in situ hybridization (FISH) and real-time quantitative PCR (RQ-PCR) were used for the diagnosis and staging of the disease. Point mutations in the tyrosine kinase domain of ABL1 gene were detected by Sanger sequencing. RESULTS: The patient was initially diagnosed as CML in chronic phase (CML-CP) with a chromosomal karyotype of 46,XX,t(5;9;22;6)(q13;q34;q11;q25), while FISH revealed presence of a variant Philadelphia chromosome translocation. Clonal evolution has occurred after 38 months of tyrosine kinase inhibitor (TKI) treatment, when cytogenetic analysis revealed coexisting t(5;9;22;6)(q13;q34;q11;q25) and t(5;9;22;6;17)(q13;q34;q11;q25;q11). After 57 months of TKIs treatment, only the t(5;9;22;6;17) clone was detected. Three months later, hyperdiploidy with additional abnormalities were detected in addition to t(5;9;22;6;17). Three mutations, including p.Tyr253Phe, p.Thr315Ile and p.Gly250Glu, were identified in the tyrosine kinase domain of the ABL1 gene during the course of disease. The patient did not attain cytogenetic and molecular response to TKIs. CONCLUSION: The four-way variant translocation may be genetically unstable. Clonal evolution and genetic mutations are likely to occur during TKIs treatment, resulting in poor response to drug therapy. This observation, however, needs to be confirmed by large-scale studies.

Correlation of anti-acetylcholine receptor antibody levels and long-term outcomes of juvenile myasthenia gravis in Taiwan: a case control study.

BACKGROUND: Myasthenia gravis is the most common disease affecting the neuromuscular junction. The most common etiology among patients with juvenile myasthenia gravis is the production of antibodies against the acetylcholine receptor. However, the clinical outcome in relation to serum levels of anti-acetylcholine receptor antibodies in juvenile myasthenia gravis has rarely been discussed. We aimed to analyze the correlation between the presence of anti-acetylcholine receptor antibodies and outcome in juvenile myasthenia gravis. METHODS: Patients diagnosed with juvenile myasthenia gravis younger than of 20 years of age were retrospectively recruited from January 1995 to February 2017 in a tertiary referral medical center. According to the Myasthenia Gravis Foundation of America outcome scale, the primary outcome was complete symptom remission and cessation of medications for at least 1 year measured 2 years after diagnosis. Secondary outcome was complete symptom remission at the last outpatient clinic. RESULTS: A total of 54 patients were followed up for over 2 years. Nine patients (9/54, 16.7%) achieved complete remission without medication use at 2 years after diagnosis. Thirteen (24.1%) patients achieved complete remission during longer follow-up periods. Those with negative anti-acetylcholine receptor antibodies were more likely to achieve complete remission at 2 years (6/15 [40%] vs. 3/39 [7.7%], 95% Confidence interval [CI] 1.670 to 38.323) and at the last outpatient clinic follow-up (8/15 [53.3%] vs. 5/39 [12.8%], 95% CI 2.367 to 20.704). Thirteen patients with comorbid autoimmune thyroid diseases were older than those without disease (11.8 ± 5.8 years old vs. 8.0 ± 6.3 years old, 95% CI 0.018 to 7.33). Moreover, patients negative for anti-acetylcholine receptor antibodies were less likely comorbid with autoimmune thyroid disease (1/35 [2.9%] vs. 12/71 [16.9%], 95% CI 0.018 to 1.161). CONCLUSIONS: Juvenile myasthenia gravis patients without anti-acetylcholine antibodies exhibited significantly increased complete remission rates and a reduced likelihood of comorbid autoimmune thyroid diseases compared with those with anti-acetylcholine receptor antibodies among Chinese.

Paeonol ameliorates monosodium urate-induced arthritis in rats through inhibiting nuclear factor-κB-mediated proinflammatory cytokine production.

Moutan Cortex has been widely used to treat various types of arthritis in traditional Chinese medicine. Paeonol is isolated as an active ingredient from Moutan Cortex. However, the effect and potential mechanism of paeonol on gouty arthritis have not been evaluated. In this study, rats were treated intragastrically with paeonol for consecutive 7 days. On Day 5, rats were intra-articularly injected with monosodium urate (MSU) crystals in the ankle joints to induce MSU-induced arthritis (MIA). Paw volume was detected at various time points. Gait score was measured at 24 hr after MSU crystal injection. Ankle joints were collected for evaluation of histological score and expression of proinflammatory cytokines using hematoxylin and eosin staining and immunohistochemistry staining, respectively. Nuclear level of nuclear factor (NF)-κBp65 in synovial tissues was analyzed by western blot assay. NF-κB DNA-binding activity was measured by enzyme linked immunosorbent assay. Paeonol markedly lowered the paw volume, gait score, and histological score in MIA rats. Mechanistically, paeonol markedly reduced the expression of TNF-α, IL-1ß, and IL-6 in synovial tissues of MIA rats. In addition, the elevated level of p65 in nucleus and NF-κB DNA-binding activity in synovial tissues of MIA rats were reduced significantly by paeonol treatment. These findings suggest that paeonol exerts anti-inflammatory effect in MIA rats through inhibiting expression of proinflammatory cytokines and NF-κB activation.

Novel laparoscopic training system with continuously perfused ex-vivo porcine liver for hepatobiliary surgery.

OBJECTIVE: To introduce a novel laparoscopic training system with a continuously perfused ex-vivo porcine liver for hepatobiliary surgery. BACKGROUND: Existing models for laparoscopic training, such as box trainers and virtual reality simulators, often fail to provide holistic training and real haptic feedback. We have formulated a new training system that addresses these problems. METHODS: Real-Liver Laptrainer consists of a porcine liver, customized mannequin, ex-vivo machine perfusion system, and monitoring software. We made a detailed comparison of Real-Liver Laptrainer with the LapSim virtual reality simulator and the FLS Trainer Box systems. Five laparoscopic surgeons assessed the new system on multiple features. We assessed the performances of 43 trainees who used the new system to perform laparoscopic cholecystectomy (LC) three times. RESULTS: Real-Liver Laptrainer offered more functions and better tactile feedback than the FLS or LapSim system. All five surgeons graded the quality of the new system as realistic. The utility of the system for training was scored as 3.6 ± 1.1 on a scale of 1-5. Between the first and third attempts, the number of successfully performed LCs increased (9 vs 14 vs 23; P = .011), while the numbers of liver damage incidents (25 vs. 21 vs. 18, P = .303) and gallbladder perforations decreased (17 vs. 12 vs. 9, P = .163). The mean LC operation time significantly decreased (63 vs. 50 vs. 44, P < .0001). CONCLUSION: Real-Liver Laptrainer is a feasible, stable, and practical training model that has potential for improving the laparoscopic skills of surgeons.

Psychomotor retardation with a 1q42.11-q42.12 deletion.

A 1q42 deletion is a rare structure variation that commonly harbours various deletion breakpoints along with diversified phenotypes. In our study, we found a de novo 1q42 deletion in a boy who did not have a cleft palate or a congenital diaphragmatic hernia but presented with psychomotor retardation. A 1.9 Mb deletion located within 1q42.11-q42.12 was validated at the molecular cytogenetic level. This is the first report of a 1q42.11-q42.12 deletion in a patient with onlypsychomotor retardation. The precise break points could facilitate the discovery of potential causative genes, such as LBR, EPHX1, etc. The correlation between the psychomotor retardation and the underlying genetic factors could not only shed light on the diagnosis of psychomotor retardation at the genetic level but also provide potential therapeutic targets.

Characterization of Cellulose Synthesis in Plant Cells.

Cellulose is the most significant structural component of plant cell wall. Cellulose, polysaccharide containing repeated unbranched ß (1-4) D-glucose units, is synthesized at the plasma membrane by the cellulose synthase complex (CSC) from bacteria to plants. The CSC is involved in biosynthesis of cellulose microfibrils containing 18 cellulose synthase (CesA) proteins. Macrofibrils can be formed with side by side arrangement of microfibrils. In addition, beside CesA, various proteins like the KORRIGAN, sucrose synthase, cytoskeletal components, and COBRA-like proteins have been involved in cellulose biosynthesis. Understanding the mechanisms of cellulose biosynthesis is of great importance not only for improving wood production in economically important forest trees to mankind but also for plant development. This review article covers the current knowledge about the cellulose biosynthesis-related gene family.

MCP-1 stimulates MMP-9 expression via ERK 1/2 and p38 MAPK signaling pathways in human aortic smooth muscle cells.

OBJECTIVE: We investigated the molecular mechanism underlying the role of monocyte chemoattractant protein-1 (MCP-1) in the formation and development of human abdominal aortic aneurysm (AAA). METHODS: We examined protein expression profiles using a protein array and found that MCP-1 was the most highly expressed protein in AAA tissues compared with normal aortas. To investigate the potential mechanism of MCP-1 involvement in the pathogenesis of AAA, we treated human aortic smooth muscle cells (HASMCs) with human recombinant MCP-1. RESULTS: MCP-1 was the most highly expressed protein in AAA tissues compared with normal aorta; matrix metalloproteinase-9 (MMP-9) expression was also significantly increased. Treatment with MCP-1 significantly increased the expression and activation of MMP-9 and activated the three major mitogen activated protein kinases (MAPKs) extracellular signal regulated kinase (ERK), c-Jun amino terminal kinase (JNK1/2) and p38 MAPK. Furthermore, MCP-1-induced secretion of MMP-9 was inhibited by U0126 (inhibitor of the ERK 1/2 pathway) and SB203580 (inhibitor of the p38 MAPK pathway), but not SP600125 (inhibitor of the JNK1/2 pathway). CONCLUSION: These data demonstrate that MCP-1 stimulates secretion of MMP-9 directly through the ERK1/2 and p38 MAPK mediated pathways in HASMCs. Thus, inhibition of this molecular mechanism might be a potential therapeutic target in the non-surgical treatment of AAA.

Effects of high extracellular K⁺ in atrium on pacemaker activity of sinoatrial node.

Sinoatrial node (SAN) plays a significant role in rhythmic firing in hearts. Little is known about the pacemaker activity of SAN when the extracellular K⁺ concentration [K⁺]o is accumulated in the atrium at the tissue level. In this paper, a gradient model of the intact SAN and its surrounding atrial muscle was developed by considering details of the SAN heterogeneous electrophysiology. The operator splitting method was used to solve the computer model. A factor k was introduced to [K⁺]o of the atrial cell to simulate the accumulation of [K⁺o. The results showed that with the elevation of [K⁺]o in the atrium, the maximum diastolic depolarization of the peripheral SANCs became less negative while their action potential amplitude became smaller than that of the control condition, but little effect was found on the central SANCs. The conduction block occurred in the atrium after [K⁺]o was elevated to greater than 2.5 times of its control condition. The larger the [K⁺]o was, the earlier the conduction block occurred. The elevation of [K⁺]o in the atrium shifted the leading pacemaker site from the center to the periphery, together with a slightly increased sinus rate. Coupling conductance within the SAN had effects on the excitation propagation in the high [K⁺]o setting. For a same [K⁺]o, the more the conductance was enhanced, the shorter the excitation propagated away from the center. In conclusion, the high [K⁺]o in the atrium was shown to modulate the pacemaker activity of SAN and impair its ability to pace and drive the atrium.

Deep learning approaches to the phylogenetic placement of extinct pollen morphotypes.

The phylogenetic interpretation of pollen morphology is limited by our inability to recognize the evolutionary history embedded in pollen features. Deep learning offers tools for connecting morphology to phylogeny. Using neural networks, we developed an explicitly phylogenetic toolkit for analyzing the overall shape, internal structure, and texture of a pollen grain. Our analysis pipeline determines whether testing specimens are from known species based on uncertainty estimates. Features from specimens with uncertain taxonomy are passed to a multilayer perceptron network trained to transform these features into predicted phylogenetic distances from known taxa. We used these predicted distances to place specimens in a phylogeny using Bayesian inference. We trained and evaluated our models using optical superresolution micrographs of 30 extant Podocarpus species. We then used trained models to place nine fossil Podocarpidites specimens within the phylogeny. In doing so, we demonstrate that the phylogenetic history encoded in pollen morphology can be recognized by neural networks and that deep-learned features can be used in phylogenetic placement. Our approach makes extinction and speciation events that would otherwise be masked by the limited taxonomic resolution of the fossil pollen record visible to palynological analysis.

Chemerin Exacerbates Psoriasis by Stimulating Keratinocyte Proliferation and Cytokine Production.

OBJECTIVE: Psoriasis is often combined with metabolic abnormalities, such as obesity and diabetes. The upregulation of chemerin, which is an essential protein produced primarily from white fat, is strongly correlated to the development of psoriasis. However, there is no clarification on its exact function and mechanism in disease pathogenesis. The present study aims to determine its function and mechanism in disease pathogenesis. METHODS: The present study used a psoriasislike inflammatory cell model and imiquimod (IMQ)-induced mouse model to confirm whether chemerin is upregulated in psoriasis patients. RESULTS: Chemerin enhanced the keratinocyte proliferation, inflammatory cytokine secretion, and activation of the MAPK signaling pathway. Crucially, the intraperitoneal injection of neutralizing anti-chemerin antibody (ChAb) diminished the epidermal proliferation and inflammation in the IMQ-induced mouse model. CONCLUSION: The present results indicate that chemerin promotes keratinocyte proliferation, and enhances the production of inflammatory cytokines, thereby aggravating the psoriasis. Thus, chemerin can be a prospective target for the treatment of psoriasis.

Normal thyroid stimulating hormone is associated with all-cause mortality in patients with acute myocardial infarction after percutaneous coronary intervention.

BACKGROUND: Circulating thyroid-stimulating hormone (TSH) levels within the normal reference range can affect the cardiovascular system. The present study investigated the prognostic value of normal TSH levels in patients presenting with acute myocardial infarction (AMI) following percutaneous coronary intervention (PCI). METHODS: Between January 2013 and July 2019, 1240 patients with AMI and normal thyroid function were enrolled and classified according to TSH tertile. The trial endpoint was all-cause mortality. The integrated discrimination index (IDI) and the net reclassification index (NRI) were used to assess the combined predictive values of the TSH levels and the Global Registry of Acute Coronary Events (GRACE) scores. RESULTS: After a median 44.25-month follow-up, 195 individuals died. Even after covariate adjustment by multivariate Cox regression (HR: 1.56; 95% CI 1.08-2.25; P = 0.017), the patients in the third TSH tertile were at the highest risk of all-cause mortality. A subgroup analysis revealed significant interactions between the TSH levels and the GRACE scores (high risk vs. low/medium risk) (P = 0.019). The addition of the TSH levels to the GRACE scores substantially improved the prediction of all-cause mortality, especially for high-risk patients (NRI = 0.239; IDI = 0.044; C-statistic value range 0.649-0.691; all significant). CONCLUSIONS: The third TSH tertile is associated with a higher incidence of all-cause mortality than the first TSH tertile in high-risk patients presenting with AMI after PCI.

Electroencephalogram pattern predicting neurological outcomes of children with seizures secondary to abusive head trauma.

BACKGROUND: The clinical presentations of abusive head trauma can abruptly worsen, so the occurrence of seizures and changes of EEG can be variable according to patients' conditions. Since the changes of EEG background waves reflect the cortical function of children, we aimed to find out whether the timing of EEG background, epileptiform discharges and seizure patterns were associated with the outcomes of patients with AHT. MATERIAL AND METHODS: Using seizure type and acute stage electroencephalographic (EEG) characteristics to assess adverse neurological outcomes in children with seizures secondary to abusive head trauma (AHT). Children who were hospitalized with AHT at a tertiary referral hospital from October 2000 to April 2010 were evaluated retrospectively. A total of 50 children below 6 years of age admitted due to AHT were included. KOSCHI outcome scale was used to evaluate the primary outcome and neurological impairment was used as secondary outcome after 6 months discharge. RESULTS: Children with apnea, cardiac arrest, reverse blood flow and skull fracture in clinic had a higher mortality rate even in the no-seizure group (3/5 [60%] vs. 3/45 [6.7%], odds ratio [OR] = 11; 95% CI = 2.3-52; p = 0.025). Seizure occurrence reduced mostly at the second day after admission in seizure groups; but children with persistent seizures for 1 week showed poor neurological outcomes. The occurrence of initial seizure was frequency associated with younger age; focal seizure, diffuse cortical dysfunction in acute-stage EEG, and low Glasgow Coma Scale (GCS) score were significantly related to poor outcomes after 6 months. Diffuse cortical dysfunction was also associated with motor, speech, and cognitive dysfunction. CONCLUSIONS: Diffuse cortical dysfunction in acute-stage EEG combined with low GCS score and focal seizure may related to poor outcomes and neurological dysfunctions in children with AHT.