Publications by authors named "Mao Ding-An"

Objective: To study the clinical features of vasovagal syncope (VVS) and postural orthostatic tachycardia syndrome (POTS) in children with neurological symptoms at disease onset.

Methods: A retrospective analysis was performed on the medical data of 88 children with the initial symptoms of the nervous system, such as transient loss of consciousness, dizziness, headache, and convulsion, who were finally diagnosed with VVS or POTS.

Results: Of the 88 children, there were 35 boys (40%) and 53 girls (60%), with an age of 4-15 years.

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Congenital myasthenic syndrome (CMS) is a group of genetic disorders of neuromuscular transmission that is characterized by muscle weakness. A mutation in the gene encoding agrin () is a rare cause of CMS, and only a few families or isolated cases have been reported. We reported a pediatric proband exhibiting muscle weakness in the trunk and limbs with skeletal malformation and intellectual disability and performed whole-exome sequencing (WES) of the proband parent-offspring trio.

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Objectives: To analyze the clinical characteristics and prognosis of children with anti-N-methyl--aspartate receptor (NMDAR) encephalitis and to provide a basis for early clinical identification of this disease.

Methods: The clinical data of 42 cases of anti-NMDAR encephalitis at Department of Pediatrics, Second Xiangya Hospital, Central South University from January 2015 to March 2018 were collected. The clinical features and followed-up outcomes were analyzed retrospectively.

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In this study, we investigated whether unique pathological characteristics exist in teratomas that can trigger autoimmune anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis. We compared a case of retroperitoneal teratoma associated with anti-NMDAR encephalitis and four control cases. The encephalitis-positive case showed that (i) more dysplastic neuroglia with higher Ki-67 labeling index values than the control cases, which met the diagnostic criteria of astrocytoma, (ii) the NMDAR subunit NR1 was expressed more abundantly in neuroglial tissue where many neuroglial cells co-expressed glial fibrillary acidic protein (GFAP) and NR1 and formed abnormally large cellular masses, (iii) intense NR1 expression occurs in squamous epithelium near neuroglial tissue and lymphocyte infiltration.

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Moyamoya disease is a chronic cerebral vascular disease characterized by progressive occlusion of the cerebral arteries and resulting in the development of abnormal collateral circulation. We report a case of moyamoya disease in a 3-year-old Chinese girl with partly reversible white matter lesions. This case indicates that, in pediatric moyamoya disease, white matter lesions may be associated with cerebral ischemia, and they may be reversible after treatment.

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Early-onset epileptic encephalopathies (EOEEs) are clinically and genetically heterogeneous disorders characterized by intractable seizures and unremitting interictal paroxysmal epileptiform activity. Consequently, these syndromes impair neurodevelopment during the first year of life. Currently, the etiology of these disorders is largely unknown.

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One of the most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxins and drug abuse is the lack of understanding the underlying mechanisms that are commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvascular endothelial cells (BMEC). Here, we hypothesized that Glycoprotein 120 (gp120), methamphetamine (METH) and nicotine (NT) can enhance amyloid-beta (Aβ) accumulation in BMEC through Alpha7 nicotinic acetylcholine receptor (α7 nAChR). Both in vitro (human BMEC) (HBMEC) and in vivo (mice) models of BBB were used to dissect the role of α7 nAChR in up-regulation of Aβ induced by gp120, METH and NT.

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Background: Recurrent convulsions can cause irreversible astrocyte death, impede neuron regeneration, and further aggravate brain damage. MicroRNAs have been revealed as players in the progression of numerous diseases including cancer and Alzheimer's disease. Particularly, microRNA has been found linked to seizure-induced neuronal death.

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Background: Epilepsy is a common neurological disorder characterized by recurrent unprovoked seizures. Seizure-induced TLR4/MYD88 signaling plays a critical role in activating microglia and triggering neuron apoptosis. SAHA is a histone deacetylase inhibitor that regulates gene expression by increasing chromatin histone acetylation.

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The pathogenesis of intractable epilepsy is not fully clear. In recent years, both animal and clinical trials have shown that the expression of ATP-binding cassette (ABC) transporters is increased in patients with intractable epilepsy; additionally, epileptic seizures can lead to an increase in the number of sites that express ABC transporters. These findings suggest that ABC transporters play an important role in the drug resistance mechanism of epilepsy.

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Objective: The aim of the study was to evaluate the effectiveness of SimBaby plus standardized patient (SP) teaching model in the simulation teaching of acute and severe bronchopneumonia in infancy.

Methods: A total of 40 students majoring in clinical medicine were assigned to either group A (SimBaby group, n = 20) or group B (SP + SimBaby group, n = 20). Medical students' expertise and their ability to apply the expertise on acute and severe bronchopneumonia in infancy were assessed using a scoring method, and the impact of the teaching model of SimBaby plus SP on medical students' comprehensive clinical capacity was assessed using a questionnaire.

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Puerarin, the main isoflavone glycoside extracted from Radix Puerariae, is an isoflavone traditional Chinese herb. Previous studies have demonstrated that puerarin could regulate osteoblast proliferation and differentiation to promote bone formation. However, the effect of puerarin on the process of human osteoblasts (hOBs) apoptosis is still unclear.

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Arterial calcification is a key pathologic component of vascular diseases such as atherosclerosis, coronary artery disease, and peripheral vascular disease. A hallmark of this pathological process is the phenotypic transition of vascular smooth muscle cells (VSMCs) to osteoblast-like cells. Several studies have demonstrated that microRNAs (miRNAs) regulate osteoblast differentiation, but it is unclear whether miRNAs also regulate VSMC-mediated arterial calcification.

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Aims: Medial artery calcification is a common macroangiopathy that initiates from a cell-regulated process similar to osteogenesis. Although the mechanisms governing this process remain unclear, epigenomic regulation by specific microRNAs might play a role in vascular smooth muscle cell (VSMC) calcification. In this study, we aimed to investigate whether miR-204 participates in the regulation of VSMC calcification.

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Objective: To investigate the behavior problems of children aged 3 to 5 years in Changsha and to compare the differences of the results detected by the norm of Conners Parent Symptom Questionnaire (PSQ) in Chinese and American urban children.

Methods: A total of 854 children aged 3 to 5 years were randomly sampled from 5 districts in Changsha City and their parents completed the Conners PSQ.

Results: The assessment by the norm of PSQ in American urban children demonstrated that the average prevalence of behavior problems was 20.

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Apoptosis of vascular smooth muscle cells (VSMCs) plays an important role in regulating vascular remodeling during cardiovascular diseases. Apelin is the endogenous ligand for the G-protein-coupled receptor APJ and plays an important role in the cardiovascular system. However, the mechanisms of apelin on apoptosis of VSMCs have not been elucidated.

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Objective: To study the changes of glucocorticoid receptor (GR) expression in embryonic rat cortical neurons exposed to transient Mg(2+)-free treatment.

Methods: Six days after rat cortical neuronal cultures, two groups were created based on the medium to which were transiently exposed. The control group was exposed to a physiological solution (PS), and the Mg(2+)-free group was exposed to the same medium as the control group except for the removal of magnesium.

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Objective: To investigate the effets of flurothyl-induced neonatal recurrent seizures on glucocorticoid receptor (GR) expression in the rat brain.

Methods: Forty-eight seven-day-old Sprague-Dawley rats were randomly divided into two groups: control and seizure. Seizures were induced by inhalant flurothyl daily for six consecutive days.

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Objective: To investigate the short-term effects of flurothyl-induced neonatal recurrent seizures on gamma-aminobutyric acid A receptor (GABAAR) alpha1 and beta2 subunit expression in the rat brain, and to study the relationship between the alterations of GABAAR subunits in the developing brain and seizure-induced brain injury.

Methods: Sixty-four 7-day-old Sprague-Dawley rats were randomly divided into two groups: control and seizure. Seizures were induced by inhalant flurothyl daily for six consecutive days.

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Objective: To investigate the long-term effects of recurrent seizures in neonate period on the expression of gamma-aminobutyric acid A receptor (GABAAR) alpha1 and beta2 subunits in brain and spatial memory and seizure susceptibility in adult period.

Methods: Thirty-two 7-day-old SD rats were randomly divided into 2 equal groups: seizure group, inhaling flurothyl to induce seizure daily for 6 days, and control group. On days 61 - 65 after birth Morris water maze test was used to record the escape latency.

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Objective: To investigate the long-term effects of flurothyl-induced neonatal recurrent seizures on GABA A receptor (GABA(A)R) alpha1 and gamma2 subunit expressions in adult rat brain, and discuss the relationship between these alterations of GABA(A)R subunits in mature brain and the changes of spatial memory and seizure susceptibility in adult rats.

Methods: Thirty-two of 7-day-old (P7) Sprague-Dawley rats were divided randomly into two groups: the control group and the seizure group. Seizures were induced by inhalant flurothyl daily for six consecutive days.

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Objective: This study investigated the effects of flurothyl-induced neonatal recurrent seizures on gamma-aminobutyric acid B1 receptor (GABAB1R) expression in neonatal and adult rat brain, and explored the possible relationship between the alterations of GABAB1R in mature brain and the changes of spatial memory and seizure susceptibility in adult rats.

Methods: Forty-eight postnatal day (P) 7 Sprague-Dawley rats were randomly assigned into two groups: Control and Seizure group (n=24 each). Seizures were induced by inhalant flurothyl daily for six consecutive days in rat pups from the Seizure group.

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Objective: The expressions of caspase-1 and cytokines activated by caspase-1 are associated with the pathophysiology of many diseases for its proinflammatory and proapototic peculiarity. However its relationship to brain injury of developing rats following recurrent seizures has not yet been identified. This study aimed to investigate the role of caspase-1 and cytokines activated by caspase-1 in brain injury of developing rats following recurrent seizures.

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