Ultrasound-targeted microbubble destruction rapidly improves left ventricular function in rats with ischemic cardiac dysfunction.

BACKGROUND: Previous studies have demonstrated the efficacy of ultrasound-targeted microbubble destruction (UTMD) in the treatment of ischemic heart failure (HF). The purpose of this study was to explore the mechanism by which UTMD improves ischemic HF. METHODS: An ischemic heart failure model was established using Sprague-Dawley rats. Rats were randomly divided into 7 groups: sham group, HF group, HF + MB group, HF + ultrasound (US) group, HF + UTMD group, HF + UTMD+LY294002 group, and HF + LY294002 group. Serum BNP level and echocardiographic parameters were measured to evaluate cardiac function. PI3K/Akt/eNOS signaling pathway protein levels were detected by immunohistochemistry (IHC) and western blotting. The concentrations of nitrous oxide (NO) and ATP were detected by ELISA, and hematoxylin and eosin (HE) staining was used to evaluate myocardial tissue. RESULTS: UTMD rapidly improved ejection fraction (EF) (HF: 37.16 ± 1.21% vs. HF + UTMD: 46.31 ± 3.00%, P < 0.01) and fractional shortening (FS) (HF: 18.53 ± 0.58% vs. HF + UTMD: 24.05 ± 1.84%, P < 0.01) in rats with ischemic HF. UTMD activated the PI3K/AKT/eNOS signaling pathway (HF vs. HF + UTMD, P < 0.01) and promoted the release of NO and ATP (HF vs. HF + UTMD, both, P < 0.05). Inhibition of the PI3K/AKT/eNOS signaling pathway by LY294002 worsened EF (HF: 37.16 ± 1.21% vs. HF + LY294002: 32.73 ± 3.05%, P < 0.05), and the release of NO and ATP by UTMD (HF + UTMD vs. HF + UTMD+LY294002, P < 0.05). CONCLUSIONS: UTMD can rapidly improve cardiac function in ischemic HF by activating the PI3K/Akt/eNOS signaling pathway and promoting the release of NO and ATP.

A case report on deficiency of adenosine deaminase 2 with relapse-remission course and analysis of genotype-phenotype correlation.

Deficiency of adenosine deaminase 2 (DADA2) is a monogenic disease caused by biallelic mutations in adenosine deaminase 2 (ADA2). The varying phenotypes of the disease often lead to delayed diagnosis or misdiagnosis. We report an 11-year-old boy with DADA2 and provide a preliminary analysis of genotype-phenotype correlation. The age of onset of the disease was 8 years old. The disease successively involved the brainstem, muscles, joints, and cerebrum. After three relapse-remission episodes over 3 years, the patient was finally diagnosed with DADA2 by whole-exome sequencing. Compound heterozygous variants in the ADA2 gene (NM_001282225.2: c.1072G>A, p.Gly358Arg; c.419dupC, p.Arg141Lysfs*37) were found in the patient. He did not receive anti-TNF therapy and had no relapse after a 8-month follow-up. We identified a novel variant of the ADA2 gene, and the associated disease course may follow a relapse-remission pattern. Homozygous mutations of p.Gly358Arg can cause pure red cell aplasia, whereas compound heterozygous variations may lead to different phenotypes. Variants in the catalytic domain and frameshift mutations may also cause relatively benign phenotypes besides causing hematological disorders. Further studies are needed to clarify the genotypic-phenotypic relationship of this disease.

Ferroptosis and Pyroptosis in Epilepsy.

Epilepsy is sudden, recurrent, and transient central nervous system dysfunction caused by abnormal discharge of neurons in the brain. Ferroptosis and pyroptosis are newly discovered ways of programmed cell death. One of the characteristics of ferroptosis is the oxidative stress generated by lipid peroxides. Similarly, pyroptosis has unique pro-inflammatory properties. As both oxidative stress and neuroinflammation are significant contributors to the pathogenesis of epilepsy, increasing evidence shows that ferroptosis and pyroptosis are closely related to epilepsy. This article reviews the current comprehension of ferroptosis and pyroptosis and elucidates potential mechanisms by which ferroptosis and pyroptosis may contribute to epilepsy. In addition, we also highlight the possible interactions between ferroptosis and pyroptosis because they reportedly coexist in many diseases, and increasing studies have demonstrated the convergence of pathways between the two. This is of great significance for explaining the occurrence and development of epilepsy and provides a new therapeutic perspective for the treatment of epilepsy.

Analysis of the relation between cerebrospinal fluid antibody titers and clinical characteristics in pediatric patients with anti-N-methyl-D-aspartate receptor encephalitis.

OBJECTIVE: This retrospective study aimed to investigate the relationship between cerebrospinal fluid (CSF) antibody titers of N-methyl-d-aspartate receptor (NMDAR), and clinical characteristics in pediatric patients with anti-NMDAR encephalitis. METHODS: The clinical and laboratory characteristics of hospitalized patients with anti-NMDAR encephalitis, stratified by antibody titers in CSF and disease severity, were retrospectively studied. The demographics, clinical characteristics, main accessory examinations, immunotherapy, and prognosis of patients were recorded, and each observed indicator was statistically analyzed. RESULTS: A total of 103 pediatric anti-NMDAR encephalitis patients were enrolled in the study, including 41 males (39.8%) and 62 females (60.2%) with a mean age of 8.0 ± 4.0 years. The proportion of patients with cognitive dysfunction and the positive pathogen was higher in the high-titer group than in the low-titer group (p = 0.023, p = 0.042). Consciousness disturbance that occurred as an initial symptom or during the course in the severe group was higher than in the non-severe group (p = 0.002, p < 0.001). More patients in the high-titer group received plasma exchange (PE) than in the low-titer group (p = 0.022). The cure rate of patients was higher with PE (65.2%) than with Corticosteroids and (or) intravenous immunoglobulin (58.1%). CONCLUSIONS: Patients with symptoms of disturbance of consciousness may be severer. The severity in pediatric anti-NMDAR encephalitis patients was not correlated with anti-NMDAR antibody titers. Patients with high CSF antibody titers had a better prognosis after early PE therapy.

Assessment of motor function and nutritional status in children with spinal muscular atrophy treated with nusinersen after loading period in Western China: a retrospective study.

BACKGROUND: Spinal muscular atrophy (SMA) is a progressive degenerative neuromuscular disease. Nusinersen, with its quick onset of action, can benefit patients early in the treatment course. However, there are currently no clinical studies regarding the improvement in motor function and nutritional status of patients after loading period treatment with nusinersen. Here, we aimed to determine the efficacy of nusinersen in improving motor function and nutritional status in children with SMA treated with nusinersen after loading period in Western China. METHODS: In this retrospective study, data for all pediatric patients (aged < 18 years), with genetically confirmed diagnosis of SMA who were treated with nusinersen, were collected before initiation of treatment and after 2 months of treatment. We assessed motor function using standardized scales and nutritional status of patients with SMA as well as side effects of nusinersen. RESULTS: Forty-six pediatric patients aged < 18 years were enrolled in this study. After 2 months of treatment, the motor function of patients with SMA type 1, 2, and 3 improved. The difference in Revised Upper Limb Module scores from M0 to M2 was significant in patients with SMA type 2 and 3 (P = 0.004, P = 0.042, respectively). The difference in Hammersmith Functional Motor Scale Expanded scores from M0 to M2 in patients with SMA type 2 was also significant (P = 0.000). No significant differences were found for Children's Hospital of Philadelphia Infant Test of Neuromuscular Disorder (CHOP-INTEND), Hammersmith Infant Neurologic Examination-Part 2 (HINE-2), and 6-Minute Walking Test (6MWT) scores between M0 and M2, but the scores of CHOP-INTEND, HINE-2, and 6MWT were all increased after loading period treatment. The overall improvement in nutritional status was not statistically significant. No serious adverse effects were observed. CONCLUSIONS: Our study provides evidence for the efficacy and safety of nusinersen and the nutritional status of pediatric patients with SMA after the loading period treatment. Motor function of all patients improved after 2 months of loading period nusinersen treatment. Patients with a shorter disease duration showed better response to treatment. Careful surveillance of nutritional status is needed in patients with SMA.

Low-Intensity Focused Ultrasound Ameliorates Ischemic Heart Failure Related to the Cholinergic Anti-Inflammatory Pathway.

OBJECTIVES: This study aims to determine the effect of low-intensity focused ultrasound (LIFU) in ischemic heart failure (IHF) and explore the potential neuroimmune mechanism. METHODS: Sprague-Dawley rats were subjected to ultrasound (US) with specific parameters, and electrocardiograms were recorded to analyze the effect of LIFU and/or vagal denervation on heart rate. Thereafter, myocardial infarction (MI) was induced by left anterior artery ligation, and LIFU was performed three times a day for 25 days after MI. Echocardiography, Masson staining, and ELISA were used to evaluate the effect of LIFU on the structure and function of the heart. Finally, ELISA, flow cytometry, qRT-PCR, and Western blot analysis were performed to determine the effect of LIFU on the inflammation and the expression of the cholinergic anti-inflammatory pathway (CAP)-related mediators. RESULTS: LIFU reduced heart rate in rats (control vs LIFU, P < .01), and vagotomy (VT) eliminated this effect of LIFU on heart rate (VT vs LIFU + VT, P > .01). LIFU-ameliorated IHF in terms of cardiac structure and function (MI vs MI + LIFU, P < .01), but VT abrogated the beneficial effect of LIFU (MI + VT vs MI + LIFU + VT, P > .01). After the treatment of LIFU, decreased levels of inflammatory cytokines, increased proportion of anti-inflammatory macrophages, and increased expression of CAP-related mediators (MI vs MI + LIFU, P < .01). CONCLUSIONS: LIFU ameliorates IHF whereas the CAP plays a promising role. LIFU has the potential to be a novel nonpharmacological and noninvasive therapy for the treatment of coronary artery disease and other cardiovascular diseases.

Novel GRIA2 variant in a patient with atypical autism spectrum disorder and psychiatric symptoms: a case report.

BACKGROUND: As sequencing technology has advanced in recent years, a series of synapse-related gene variants have been reported to be associated with autism spectrum disorders (ASDs). The α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor is a subtype of the ionotropic glutamate receptor, whose number or composition changes can regulate the strength and plasticity of synapses. CASE PRESENTATION: Here, we report a de novo GRIA2 variant (NM_001083619.3: c.2308G > A, p.Ala770Thr) in a patient with obvious behavior regression and psychiatric symptoms. It encodes GluA2, which is the crucial subunit of the AMPA receptor, and the missense variation is predicted to result in instability of the protein structure. CONCLUSIONS: The association between GRIA2 variants and onset of ASD symptoms is rare, and our study expands the spectrum of phenotypic variations. For patients with an unexplained etiology of ASD accompanied by psychiatric symptoms, genetic causes should be considered, and a complete genetic evaluation should be performed.

Clinical implementation of ketogenic diet in children with drug-resistant epilepsy: Advantages, disadvantages, and difficulties.

PURPOSE: Ketogenic diet (KD) is a well-established nonpharmacologic treatment for drug-resistant epilepsy. However, although KD has a long history of clinical use, there are still many difficulties with its real-world practice. This study retrospectively described the situation of KD practice in two children's hospitals in Southwest China. METHODS: We reviewed and analyzed clinical data collected at the baseline, and during follow ups at 1, 3, 6, 12, 18, and 24 months. The patient retention, the efficacy, side effects of KD, and the reasons for discontinuation were focused. RESULTS: There was increasing availability of KD for children with epilepsy in Southwest China and its effectiveness in controlling seizures was reconfirmed. Nonetheless, less than half of the patients adhered to KD for one year and about 1/5 of the patients for two years. Unsatisfactory seizure control was the most common reason for discontinuation, followed by patient/caregiver preference, acute infection, and loss to follow up. Adverse effects were mostly tolerable and not the main reason for discontinuation. Meanwhile, KD showed negative impacts on linear growth, and our cohort seemed to have more infections and deaths. CONCLUSIONS: Despite increasing availability and good efficacy, long-term adherence to KD was difficult. Compliance issues appeared to be prominent. Enhancing food taste and patient support can help to improve the retention rate.

Gut flora and metabolism are altered in epilepsy and partially restored after ketogenic diets.

OBJECTIVE: The aim of this study was to investigate the composition of the intestinal microbiota and its association with fecal short chain fatty acids (SCFAs) in children with drug refractory epilepsy (DRE) before and after treatment with a ketogenic diet (KD). METHODS: Herein, we conducted a cross-sectional study of 12 children with DRE and 12 matched healthy controls to compare the changes in fecal microbiomes and SCFAs. Disease cohort also underwent analysis before and after 6 months of KD treatment. RESULTS: A higher microbial alpha diversity and a significant increase in Actinobacteria at the phylum level and Enterococcus, Anaerostipes, Bifidobacterium, Bacteroides, and Blautia at the genus level were observed in the children with DRE. The abundance of the eight epileptic-associated genera was reversed after six months of KD treatment with decreases in Bifidobacterium, Akkermansia, Enterococcaceae and Actinomyces and increases in Subdoligranulum, Dialister, Alloprevotella (p < 0.05). In particular, we identified some taxa that were more prevalent in patients with an inadequate response to KD than in those with an adequate response. Further, a significant correlation was observed between the change in the microbiome genera after KD treatment. The SCFA content in the fecal after 6 months of KD treatment increased and was highly correlated with the gut bacteria. SIGNIFICANCES: Dysbiosis of the microbiome could be involved in the pathogenesis of DRE in children, which can be relieved by a KD to a large extent. Gut microbiota and microbial metabolism could contribute to the antiseizure effect of KD.

miR-384-5p promotes spinal cord injury recovery in rats through suppressing of autophagy and endoplasmic reticulum stress.

BACKGROUND: Spinal cord injury (SCI) is one of the most serious neurological disorders and is characterized by high morbidity and disability. Unfortunately, there is a lack of effective treatment. Recently, the micro RNA, miR-384-5p, was reported to play a significant role in cell survival in response to different insults. METHODS: In vitro model of traumatic neuronal injury was induced by application of a sharp sterile blade to generate cuts in PC12 cells, and in vivo SCI was produced by applying vascular clips (force of 15 g) to the dura via T9-T10 laminectomy, and then, the role of miR-384-5p in the development of SCI was investigated. RESULTS: Dual-luciferase reporter assays confirmed that miR-384-5p regulates the gene expression of Beclin-1, an important promoter of autophagy. Quantitative polymerase chain reaction and western blot analyses revealed that treatment with miR-384-5p decreased mRNA and protein expression of Beclin-1 in the mechanically injured PC12 cells. In rats with spinal cord compression injuries, miR-384-5p expression was significantly decreased. Treatment with miR-384-5p increased spinal cord neuron survival and promoted locomotor function recovery in rats. Further study revealed that miR-384-5p administration decreased immunofluorescent labeling of Beclin-1 in spinal cord tissues and reduced autophagosome formation in neurons, as shown by transmission electron microscopy. These results indicated that miR-384-5p promotes recovery of rats with SCI by suppressing autophagy via direct targeting of Beclin-1. Moreover, miR-384-5p also inhibited the activation of endoplasmic reticulum (ER) stress by decreasing GRP78 expression in both in vitro and in vivo models. CONCLUSIONS: This study for the first time demonstrates that the protective role of miR-384-5p in the process of SCI is associated with simultaneous suppression of autophagy and ER stress and miR-384-5p could be a promising candidate for SCI therapeutics.

Expression and functional analysis of lncRNAs in the hippocampus of immature rats with status epilepticus.

Long non-coding RNAs (lncRNAs) have been implicated in the regulation of gene expression at various levels. However, to date, the expression profile of lncRNAs in status epilepticus (SE) was unclear. In our study, the expression profile of lncRNAs was investigated by high-throughput sequencing based on a lithium/pilocarpine-induced SE model in immature rats. Furthermore, weighted correlation network analysis (WGCNA), gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed to construct co-expression networks and establish functions of the identified hub lncRNAs in SE. The functional role of a hub lncRNA (NONRATT010788.2) in SE was investigated in an in vitro model. Our results indicated that 7082 lncRNAs (3522 up-regulated and 3560 down-regulated), which are involved in cell proliferation, inflammatory responses, angiogenesis and autophagy, were dysregulated in the hippocampus of immature rats with SE. Additionally, WGCNA identified 667 up-regulated hub lncRNAs in turquoise module that were involved in apoptosis, inflammatory responses and angiogenesis via regulation of HIF-1, p53 and chemokine signalling pathways and via inflammatory mediator regulation of TRP channels. Knockdown of an identified hub lncRNA (NONRATT010788.2) inhibited neuronal apoptosis in vitro. Taken together, our study is the first to demonstrate the expression profile and potential function of lncRNAs in the hippocampus of immature rats with SE. The defined hub lncRNAs may participate in the pathogenesis of SE via lncRNA-miRNA-mRNA network.

Mapping the knowledge structure and trends of epilepsy genetics over the past decade: A co-word analysis based on medical subject headings terms.

INTRODUCTION: Over the past 10 years, epilepsy genetics has made dramatic progress. This study aimed to analyze the knowledge structure and the advancement of epilepsy genetics over the past decade based on co-word analysis of medical subject headings (MeSH) terms. METHODS: Scientific publications focusing on epilepsy genetics from the PubMed database (January 2009-December 2018) were retrieved. Bibliometric information was analyzed quantitatively using Bibliographic Item Co-Occurrence Matrix Builder (BICOMB) software. A knowledge social network analysis and publication trend based on the high-frequency MeSH terms was built using VOSviewer. RESULTS: According to the search strategy, a total of 5185 papers were included. Among all the extracted MeSH terms, 86 high-frequency MeSH terms were identified. Hot spots were clustered into 5 categories including: "ion channel diseases," "beyond ion channel diseases," "experimental research & epigenetics," "single nucleotide polymorphism & pharmacogenetics," and "genetic techniques". "Epilepsy," "mutation," and "seizures," were located at the center of the knowledge network. "Ion channel diseases" are typically in the most prominent position of epilepsy genetics research. "Beyond ion channel diseases" and "genetic techniques," however, have gradually grown into research cores and trends, such as "intellectual disability," "infantile spasms," "phenotype," "exome," " deoxyribonucleic acid (DNA) copy number variations," and "application of next-generation sequencing." While ion channel genes such as "SCN1A," "KCNQ2," "SCN2A," "SCN8A" accounted for nearly half of epilepsy genes in MeSH terms, a number of additional beyond ion channel genes like "CDKL5," "STXBP1," "PCDH19," "PRRT2," "LGI1," "ALDH7A1," "MECP2," "EPM2A," "ARX," "SLC2A1," and more were becoming increasingly popular. In contrast, gene therapies, treatment outcome, and genotype-phenotype correlations were still in their early stages of research. CONCLUSION: This co-word analysis provides an overview of epilepsy genetics research over the past decade. The 5 research categories display publication hot spots and trends in epilepsy genetics research which could consequently supply some direction for geneticists and epileptologists when launching new projects.

The role of necroptosis in status epilepticus-induced brain injury in juvenile rats.

PURPOSE: To study the role of necroptosis in status epilepticus (SE)-induced injury in the developing brain and the possible associations of necroptosis with epileptogenesis and cognitive dysfunction. METHODS: The lithium-pilocarpine epilepsy model was reproduced in male rats at postnatal day 25. Propidium iodide (PI) staining was used to detect cell death after SE. Transmission electron microscopy (TEM) was performed to observe morphological changes in injured neurons. Western blot and immunofluorescence (IF) staining were used to investigate the expression of receptor interacting protein kinase-3 (RIP3), mixed lineage kinase domain-like (MLKL), and p-MLKL after SE. EEG was monitored during the chronic epileptic period. The Morris water maze test was performed to evaluate spatial learning and memory in juvenile rats after SE. RESULTS: Massive PI-positive (PI+) neurocytes were observed mainly in the amygdala and piriform cortex 24h to 7days after SE, with the most prominent changes observed after 72h. Injured neurons observed via TEM exhibited necroptotic morphological features, including loss of ribosomes, autophagosome formations, deformed nuclei with condensed and marginated chromatin, and disruptive cell membranes. The expression of RIP3 and p-MLKL increased after 24h, peaked at 72h, and decreased 7days after SE. In addition, IF staining revealed that MLKL was expressed in cell plasma membranes present in the amygdala and piriform cortex. This finding was concomitant with the fact that MLKL is involved in executing necroptosis by binding and disrupting the plasma membrane. During the chronic epileptic period, spontaneous recurrent seizures were observed behaviorally and interictal spikes and sharp waves were recorded by EEG in the SE group. The Morris water maze test revealed that in the place navigation test, the escape latency of the SE group was longer than that of the control group (p<0.05). In the spatial probe test, the number of times the rats in the SE group passed through the original platform site was lesser than that of the rats in the control group (p<0.05). CONCLUSION: SE-induced brain injury leads to neuronal necroptosis in juvenile rats. MLKL may play a significant role in the execution of SE-induced necroptosis. Further studies are required to determine whether inhibiting necroptosis can prevent chronic epileptogenesis and improve cognitive ability for juvenile rats.

miR-96 attenuates status epilepticus-induced brain injury by directly targeting Atg7 and Atg16L1.

Status epilepticus (SE) can cause brain damage and lead to neural dysfunction. Developing novel targets for SE therapy and diagnosis is important and necessary. Previously, we found several differentially expressed microRNAs (miRNAs) in the developing hippocampus following SE, including the autophagy-related miR-96. In the present study, we employed immunofluorescence staining and Western blot analysis to assess the expression of autophagy-related 7 (Atg7) and Atg16L1 and the status of autophagosome formation in the hippocampus of immature rats with SE. Additional in vivo intervention was also performed to investigate the potential therapeutic function of miR-96 in developing rats with SE. We found that Atg7 and Atg16L1 were up-regulated in the neurons after SE, together with an increase in autophagosome formation. Meanwhile, overexpression of miR-96 significantly prevented brain damage in SE rats by inhibiting Atg7 and Atg16L1 expression and autophagosome formation in the hippocampus. Furthermore, Rapamycin negated miR-96 mediated brain injury attenuation through inducing autophagosome formation. Our study indicates that miR-96 might be a potential target for therapy of pediatric SE.

Safety and tolerability of the ketogenic diet used for the treatment of refractory childhood epilepsy: a systematic review of published prospective studies.

BACKGROUND: To review the available evidence from prospective studies on the safety and tolerability of the ketogenic diet (KD) for the treatment of refractory childhood epilepsy. METHODS: A comprehensive bibliographic search was performed with the aim of retrieving prospective studies that monitored adverse effects (AEs) in children after receiving the classic or medium-chain triglyceride KD therapy for refractory epilepsy. RESULTS: A total of 45 studies were retrieved, including 7 randomized controlled trials. More than 40 categories of AEs were reported. The most common AEs included gastrointestinal disturbances (40.6%), hyperlipidemia (12.8%), hyperuricemia (4.4%), lethargy (4.1%), infectious diseases (3.8%) and hypoproteinemia (3.8%). Severe AEs, such as respiratory failure and pancreatitis, occurred in no more than 0.5% of children. Specifically, patients receiving KD therapy should be monitored for osteopenia, urological stones, right ventricular diastolic dysfunction, and growth disturbance. The total retention rates of the diet for 1 year and 2 years were 45.7% and 29.2%, respectively. Nearly half of the patients discontinued the diet because of lack of efficacy. AEs were not the main reason for the KD discontinuation. None of the 24 deaths reported after initiation of the diet was attributed to the KD. CONCLUSIONS: KD is a relatively safe dietary therapy. However, because the KD can cause various AEs, it should be implemented under careful medical supervision. Continuous follow-up is needed to address the long-term impact of the diet on the overall health of children.

Visualization and quantitation of fetal movements by real-time three-dimensional ultrasound with live xPlane imaging in the first trimester of pregnancy.

AIM: To prove whether real-time three-dimensional (3D) ultrasound with live xPlane imaging is better in observing fetal movements than standard ultrasound imaging. METHODS: 50 healthy women with singleton pregnancies (22-43 years old) at 11 to 14 weeks of gestation underwent real-time 3D ultrasound examination with live xPlane imaging from July 2014 to February 2015. The incidence and frequency of 10 fetal movement patterns in 10 minutes were evaluated, including general movements (GMs), isolated arm movements, isolated leg movements, hiccup, stretching, breathing, startle, jaw opening, isolated head retroflexion, and isolated head anteflexion. The correlation between gestational age and frequency of each fetal movement pattern was analyzed. RESULTS: GM had the highest incidence (100%), followed by startle (84%) and isolated arm movements (68%). Their median frequency was 5 (IQR 3-6), 5 (IQR 1.75-11.5), and 1 (IQR 0-2), respectively. GM (Z=5.875, P<0.001) and startle (Z=5.302, P<0.001) had significantly higher frequency than isolated arm movements. The other 7 fetal movement patterns had much lower incidence and frequency. The frequency of GM was positively correlated with gestational age (r=0.360, P=0.010). CONCLUSION: Real-time 3D ultrasound with live x Plane imaging was shown to be a feasible tool for observing fetal movements.

A Cross-sectional Survey of Growth and Nutritional Status in Children With Cerebral Palsy in West China.

BACKGROUND: We describe the growth and nutritional status of children with cerebral palsy (2 to 18 years old) in West China and to explore the correlation between the nutritional status and age, gender, and gross and fine motor function. METHODS: We performed a cross-sectional survey of children registered as having cerebral palsy in the China Disabled Persons' Federation branch in Chengdu. Growth (height and weight) and nutritional (body mass index) status were recorded. Gross Motor Function Classification System (GMFCS) and Manual Ability Classification System (MACS) were used to determine gross and fine motor function, respectively. The association between nutritional status and age, GMFCS and MACS levels was evaluated. RESULTS: We enrolled 377 children (53.6% male), among whom 160 (42.4%) were stunting, 48 (12.7%) underweight, 81 (21.5%) thin, and 70 (18.5%) overweight and obese. Thinness was the main nutritional problem in older patients (12 to 18 years), whereas overweight and obesity were the major issues in younger patients (2 to 12 years). Growth deviation and malnutrition were significantly more prevalent in patients with severe motor impairments. A significant negative correlation was found between nutritional status and age, GMFCS and MACS levels, and between growth and GMFCS and MACS levels. CONCLUSIONS: Growth abnormality is common in children with cerebral palsy. Malnutrition and overnutrition both exist in children with cerebral palsy. Characteristics at different age stages and motor functional levels should be taken into consideration in the management of growth and nutrition in this population.

Kawasaki disease mimicking a parapharyngeal abscess: a case report.

Parapharyngeal abscess (PPA)-like lesion is a very rare manifestation of Kawasaki disease (KD). Here we report a Chinese case of KD initially mimicking PPA, which is the first one reported in Asia.A 3-year-old male patient presented with fever, drooling, and bilateral painful cervical lymphadenopathy for 3 days. Chest X-ray and echocardiogram were normal. With substantial elevation of white blood count and C-reactive protein, purulent cervical lymphadenitis was considered. Symptoms did not improve after treatment with vancomycin, and the patient further developed trismus and restricted neck movement. Neck CT revealed a 2 × 1.5 cm hypodense lesion in the right parapharyngeal space with peripheral enhancement. PPA was suspected and on the 3rd day following admission, the patient received surgical incision and drainage. One milliliter of serous fluid was drained without bacterial growth on cultures. Fever persisted after surgery. As the clinical course proceeded, additional major signs of KD gradually evolved, and on the 6th day following admission the patient completely fulfilled the diagnostic criteria for KD. Rapid clinical improvement was observed following treatment with high-dose immunoglobulin and aspirin. Due to the parapharyngeal operation, the patient was fed milk through a nasogastric tube for 15 days. His neck incision became infected but healed gradually following dressing change and antibiotic treatment. Currently he remains asymptomatic during regular follow-up and repeated echocardiograms are normal.Both pediatricians and otolaryngologists can learn from this case that KD may initially manifest as PPA. Careful observation for major signs of KD during the clinical course can help to achieve a prompt and correct diagnosis. Thus, unnecessary surgery and cardiac complications of KD may be avoided.