A Wearable Self-Charging Electroceutical Device for Bacteria-Infected Wound Healing.

The prolonged wound-healing process caused by pathogen infection remains a major public health challenge. The developed electrical antibiotic administration typically requires metal electrodes wired to a continuous power supply, restricting their use beyond clinical environments. To obviate the necessity for antibiotics and an external power source, we have developed a wearable synergistic electroceutical device composed of an air self-charging Zn battery. This battery integrates sustained tissue regeneration and antibacterial modalities while maintaining more than half of the initial capacity after ten cycles of chemical charging. In vitro bacterial/cell coculture with the self-charging battery demonstrates inhibited bacterial activity and enhanced cell function by simulating the endogenous electric field and dynamically engineering the microenvironment with released chemicals. This electroceutical device provides accelerated healing of a bacteria-infected wound by stimulating angiogenesis and modulating inflammation, while effectively inhibiting bacterial growth at the wound site. Considering the simple structure and easy operation for long-term treatment, this self-charging electroceutical device offers great potential for personalized wound care.

An insertion mutation of the MECP2 gene in severe neonatal encephalopathy and ocular and oropharyngeal dyskinesia: a case report.

BACKGROUND: Pathogenic variation of the MECP2 gene presents mostly as Rett syndrome in females and is extremely rare in males. Most male patients with MECP2 gene mutation show MECP2 duplication syndrome. CASE PRESENTATION: Here we report a rare case in a 10-month-old boy with a hemizygous insertion mutation in MECP2 as NM_001110792, c.799_c.800insAGGAAGC, which results in a frameshift mutation (p.R267fs*6). The patient presented with severe encephalopathy in the neonatal period, accompanied by severe development backwardness, hypotonia, and ocular and oropharyngeal dyskinesia. This is the first report of this mutation, which highlights the phenotype variability associated with MECP2 variants. CONCLUSIONS: This case helps to expand the clinical spectrum associated with MECP2 variants. Close attention should be paid to the growth and development of patients carrying a MECP2 variant or Xq28 duplication. Early interventions may help improve symptoms to some certain extent.

Electroclinical characteristics of photosensitive epilepsy: A retrospective study of 31 Chinese children and literature review.

Objective: The objective of this study was to better understand the clinical features of photosensitive epilepsy (PSE) in Chinese children. Methods: Thirty-one children with PSE were screened out of 398 children with epilepsy who were consecutively diagnosed by the video-electroencephalogram (VEEG) monitoring method and by using an intermittent photic stimulation (IPS) test. Their EEGs and clinical features were retrospectively analyzed, and their treatment outcomes were followed up. Results: PSE accounted for 7.79% (31/398) of children with epilepsy during the observation period in our single epilepsy center. The male to female ratio of PSE was 1:3.43, and the average seizure onset age was 7.8 ± 3.28 years. The highest range of frequency sensitivity of the IPS test for the induction of EEG epileptic discharge or electroclinical seizures was within 10-20 Hz. Electroclinical seizures were induced in 41.94% (13/31) of PSE patients by using the IPS test, while EEG discharge without clinical seizures was induced in 58.06% (18/31) of PSE patients. Among all PSE patients, an IPS-positive reaction in the eye-closure state was induced in 83.87% of patients, and this rate was significantly higher than that in the eye-opened state (41.94%) or eye-closed state (35.48%). (Eye-closure IPS stimulation means: make the subjects close their eyes at the beginning of each stimulation, open their eyes at the end of the stimulation, and close their eyes again at the beginning of the next stimulation, and so on. While Eye-closed IPS stimulation means the stimulation is started after 5 s of eye closure, and the subjects are kept closed throughout the whole process.) The common and effective drugs used for single or combined therapy in PSE children were valproic acid and levetiracetam. Conclusion: This study provides some useful information about electroclinical characteristics in a cohort of 31 PSE children. It may be beneficial for pediatric neurologists in terms of paying more attention to PSE and correctly dealing with it.

A biocompatible and fully erodible conducting polymer enables implanted rechargeable Zn batteries.

Implanted rechargeable batteries that can provide energy over a sufficient lifetime and ultimately degrade into non-toxic byproducts are highly desirable. However, their advancement is significantly impeded by the limited toolbox of electrode materials with a known biodegradation profile and high cycling stability. Here we report biocompatible, erodible poly(3,4-ethylenedioxythiophene) (PEDOT) grafted with hydrolyzable carboxylic acid pendants. This molecular arrangement combines the pseudocapacitive charge storage from the conjugated backbones and dissolution via hydrolyzable side chains. It demonstrates complete erosion under aqueous conditions in a pH-dependent manner with a predetermined lifetime. The compact rechargeable Zn battery with a gel electrolyte offers a specific capacity of 31.8 mA h g-1 (57% of theoretical capacity) and outstanding cycling stability (78% capacity retention over 4000 cycles at 0.5 A g-1). Subcutaneous implantation of this Zn battery into Sprague-Dawley (SD) rats demonstrates complete biodegradation in vivo and biocompatibility. This molecular engineering strategy presents a viable avenue for developing implantable conducting polymers with a predetermined degradation profile and high energy storage capability.

Childhood absence epilepsy patients with cognitive impairment have decreased sleep spindle density.

OBJECTIVE: To explore the differences in sleep spindle (SS) characteristics during stage N2 sleep between children with childhood absence epilepsy and healthy controls, and between children with childhood absence epilepsy with or without cognitive impairment. METHODS: We recruited 29 children (14 females, 15 males, mean age: 8 (2.5) years) with childhood absence epilepsy who did not undergone antiseizure treatments previously and 30 age-matched controls (14 females, 16 males, mean age: 9 (3.0) years). For all patients, data on medical history were collected. Each child was monitored overnight by long-term video electroencephalography and was evaluated by the Wechsler Intelligence Scale for Children-Fourth Edition. Next, we compared anterior SS characteristics, including density, frequency, cycle length, duration, amplitude, and percentage of sleep stages. RESULTS: The childhood absence epilepsy group exhibited lower spindle density and duration in the first 37.5 min of stage N2 sleep than the control group (P < 0.01). A decrease in spindle density could be observed in the childhood absence epilepsy group with aggravated cognition impairment. The spindle density was substantially lower in the cognitively impaired group than in the cognitively unimpaired group (P < 0.01). No significant differences were observed in SS amplitude, SS frequency, SS cycle length, and the distribution of sleep stages. CONCLUSIONS: Reduction in spindle density and duration is associated with the mechanisms underlying childhood absence epilepsy. The deficit in SS density is related with impaired cognition. This deficiency in SSs may be a useful predictive indicator of cognitive impairment in children with absence epilepsy, indicating that SSs may become a useful biomarker and potential adjuvant anti-seizure target for cognitive impairment caused by childhood absence epilepsy.

Review Cerebral Ischemic Tolerance and Preconditioning: Methods, Mechanisms, Clinical Applications, and Challenges.

Stroke is one of the leading causes of morbidity and mortality worldwide, and it is increasing in prevalence. The limited therapeutic window and potential severe side effects prevent the widespread clinical application of the venous injection of thrombolytic tissue plasminogen activator and thrombectomy, which are regarded as the only approved treatments for acute ischemic stroke. Triggered by various types of mild stressors or stimuli, ischemic preconditioning (IPreC) induces adaptive endogenous tolerance to ischemia/reperfusion (I/R) injury by activating a multitude cascade of biomolecules, for example, proteins, enzymes, receptors, transcription factors, and others, which eventually lead to transcriptional regulation and epigenetic and genomic reprogramming. During the past 30 years, IPreC has been widely studied to confirm its neuroprotection against subsequent I/R injury, mainly including local ischemic preconditioning (LIPreC), remote ischemic preconditioning (RIPreC), and cross preconditioning. Although LIPreC has a strong neuroprotective effect, the clinical application of IPreC for subsequent cerebral ischemia is difficult. There are two main reasons for the above result: Cerebral ischemia is unpredictable, and LIPreC is also capable of inducing unexpected injury with only minor differences to durations or intensity. RIPreC and pharmacological preconditioning, an easy-to-use and non-invasive therapy, can be performed in a variety of clinical settings and appear to be more suitable for the clinical management of ischemic stroke. Hoping to advance our understanding of IPreC, this review mainly focuses on recent advances in IPreC in stroke management, its challenges, and the potential study directions.

The efficacy and safety of salvianolic acids on acute cerebral infarction treatment: A protocol for systematic review and meta analysis.

BACKGROUND: Salvianolic acids (SA) has been widely used for the treatment of acute cerebral infarction (ACI) combined with basic western medicine therapy in China. This study was aimed to evaluate the efficacy and safety of SA on ACI treatment and its influence on neurological functions, activity of daily living, and cognitive functions. METHODS: We retrieved related articles from PubMed, the Cochrane Center Controlled Trials Register, EMBASE, Medline, Ovid, Chinese National Knowledge Infrastructure, Chinese Biomedical Literature Database, and Wanfang Database without date and language restrictions. Finally, 58 randomized controlled trials were included from 239 retrieved records. Two researchers extracted the basic information and data from included articles and assessed the quality and analysis of data by using Review Manager 5.3. RESULTS: The administration of SA significantly increased the total clinical effective rate of ACI treatment (P < .001) and improved the National Institute of Health Stroke Scale scores, modified Rankin Scale scores, and Barthel Index scores after treatment and 3 months after ACI (P < .05). The activities of daily living scores in the SA group were significantly increased after treatment (P < .001), whereas they were remarkably decreased 3 months after ACI (P < .001) compared with that in the control group. Besides, SA profoundly promoted the recovery of Montreal Cognitive Assessment scores (P < .001). However, the use of SA increased the risk of adverse events occurrence (P = .007). CONCLUSION: SA combined with basic western medicine treatment could promote neurological functions, daily living activities, and cognitive functions recovery of ACI patients. Although SA increased the risk of adverse events occurrence, these adverse events were easily controlled or disappeared spontaneously.

Mechanisms underlying astrocytic connexin-43 autophagy degradation during cerebral ischemia injury and the effect on neuroinflammation and cell apoptosis.

Connexin-43 (Cx43) is the most abundant gap junction protein in the nervous system. It enables cell communication and has important physiological roles including ion transport and substrate exchange, all of which have been implicated in cerebral ischemia injury. Our previous in vitro and in vivo studies have demonstrated that Cx43 is internalized and degraded during ischemia stress. However, the significance of ischemia-induced degradation of Cx43 remains unclear. Herein, we demonstrated that Cx43 degradation during ischemia injury is mediated by selective autophagy; additionally, we identified two related autophagy receptors-OPTN and NDP52. Cx43 degradation during ischemia requires its phosphorylation and ubiquitination, which are mediated by PKC, Src kinases, and ubiquitin kinase PINK1. Using point mutagenesis, we identified three phosphorylation sites underlying Cx43 autophagy degradation under ischemic stress. Cx43 degradation inhibition promoted the transition of astrocytes from a pro-inflammatory to an anti-inflammatory status, based on the levels of IL-10 and TNF in ischemia. Knockdown or accelerated degradation of Cx43 protected astrocytes from apoptosis under ischemic stress. These findings elucidate the underlying mechanism of astrocytic Cx43 autophagic degradation during ischemia. The study has identified potentially novel therapeutic strategies against ischemic stroke and evidence of crosstalk between autophagic degradation of Cx43, astrocytic apoptosis, and neuroinflammation.

Cyclic adenosine monophosphate in acute ischemic stroke: some to update, more to explore.

The development of effective treatment for ischemic stroke, which is a common cause of morbidity and mortality worldwide, remains an unmet goal because the current first-line treatment management interventional therapy has a strict time window and serious complications. In recent years, a growing body of evidence has shown that the elevation of intracellular and extracellular cyclic adenosine monophosphate (cAMP) alleviates brain damage after ischemic stroke by attenuating neuroinflammation in the central nervous system and peripheral immune system. In the central nervous system, upregulated intracellular cAMP signaling can alleviate immune-mediated damage by restoring neuronal morphology and function, inhibiting microglia migration and activation, stabilizing the membrane potential of astrocytes and improving the cellular functions of endothelial cells and oligodendrocytes. Enhancement of the extracellular cAMP signaling pathway can improve neurological function by activating the cAMP-adenosine pathway to reduce immune-mediated damage. In the peripheral immune system, cAMP can act on various immune cells to suppress peripheral immune function, which can alleviate the inflammatory response in the central nervous system and improve the prognosis of acute cerebral ischemic injury. Therefore, cAMP may play key roles in reducing post-stroke neuroinflammatory damage. The protective roles of the cAMP indicate that the cAMP enhancing drugs such as cAMP supplements, phosphodiesterase inhibitors, adenylate cyclase agonists, which are currently used in the treatment of heart and lung diseases. They are potentially able to be applied as a new therapeutic strategy in ischemic stroke. This review focuses on the immune-regulating roles and the clinical implication of cAMP in acute ischemic stroke.

Inflammation resolution and specialized pro-resolving lipid mediators in CNS diseases.

Introduction: Inflammation resolution induced by specialized pro-resolving lipid mediators (SPMs) is a new concept. The application of SPMs is a promising therapeutic strategy that can potentially supersede anti-inflammatory drugs. Most CNS diseases are associated with hyperreactive inflammatory damage. CNS inflammation causes irreversible neuronal loss and permanent functional impairments. Given the high mortality and morbidity rates, the investigation of therapeutic strategies to ameliorate inflammatory damage is necessary.Areas covered: In this review, we explore inflammation resolution in CNS disorders. We discuss the underlying mechanisms and dynamic changes of SPMs and their precursors in neurological diseases and examine how this can potentially be incorporated into the clinic. References were selected from PubMed; most were published between 2010 and 2019.Expert opinion: Inflammation resolution is a natural process that emerges after acute or chronic inflammation. The evidence that SPMs can effectively ameliorate hyperreactive inflammation, shorten resolution time and accelerate tissue regeneration in CNS disorders. Adjuvants and nanotechnology offer opportunities for SPM drug design; however, more preclinical studies are necessary to investigate basic, critical issues such as safety.

Myelopathy associated with mixed connective tissue disease: clinical manifestation, diagnosis, treatment, and prognosis.

Mixed connective tissue disease (MCTD) is a chronic autoimmune disease, which has a broad range of clinical manifestations shared by systemic lupus erythematosus, systemic sclerosis, polymyositis/dermatomyositis, and rheumatoid arthritis. MCTD is featured with high serum titers of anti-ribonucleoprotein antibodies and multiple system involvement. Its spinal cord involvement mainly manifests as transverse myelopathy (TM) and longitudinal extensive transverse myelopathy (LETM). Myelopathy in MCTD is extremely rare, and is usually characterized by serious neurological complications, such as paralysis or muscular paresis, sensory impairment, and smooth muscle dysfunction. Progressive clinical manifestations combined with laboratory examinations and magnetic resonance imaging examinations play important roles in the diagnosis of this disease. In order to prevent permanent neurological damage to the spinal cord, plasmapheresis and intravenous immunoglobulin can be performed in patients at the early disease stage. Early high-dose corticosteroids combined with cyclophosphamide, followed by low doses of immunosuppressors, can improve the long-term prognosis of patients. There are only nine global cases reported on MCTD associated with myelopathy at present. The death rate and disability rate of myelopathy in MCTD are extremely high. In this review, the pathomechanisms, clinical manifestations, auxiliary examination, diagnosis, differential diagnosis, treatment, and prognosis of myelopathy in MCTD were systematically elucidated.

Potential Applications of Remote Limb Ischemic Conditioning for Chronic Cerebral Circulation Insufficiency.

Chronic cerebral circulation insufficiency (CCCI) refers to a chronic decrease in cerebral blood perfusion, which may lead to cognitive impairment, psychiatric disorders such as depression, and acute ischemic stroke. Remote limb ischemic conditioning (RLIC), in which the limbs are subjected to a series of transient ischemic attacks, can activate multiple endogenous protective mechanisms to attenuate fatal ischemic injury to distant organs due to acute ischemia, such as ischemic stroke. Recent studies have also reported that RLIC can alleviate dysfunction in distant organs caused by chronic, non-fatal reductions in blood supply (e.g., CCCI). Indeed, research has indicated that RLIC may exert neuroprotective effects against CCCI through a variety of potential mechanisms, including attenuated glutamate excitotoxicity, improved endothelial function, increased cerebral blood flow, regulation of autophagy and immune responses, suppression of apoptosis, the production of protective humoral factors, and attenuated accumulation of amyloid-ß. Verification of these findings is necessary to improve prognosis and reduce the incidence of acute ischemic stroke/cognitive impairment in patients with CCCI.

Cerebral Ischemic Postconditioning Plays a Neuroprotective Role through Regulation of Central and Peripheral Glutamate.

Following cerebral ischemia/reperfusion (I/R) injury, a series of pathophysiological processes are stimulated in both the central nervous system (CNS) and the periphery, including, but not limited to, the peripheral immune and endocrine systems and underregulation of the neuroendocrine-immune network. Glutamate (Glu) is an important excitatory neurotransmitter in the CNS; its excitotoxicity following cerebral ischemia has been a focus of study for several decades. In addition, as a novel immunoregulator, Glu also regulates immune activity in both the CNS and periphery and may connect the CNS and periphery through regulation of the neuroendocrine-immune network. Ischemic postconditioning (IPostC) is powerful and activates various endogenous neuroprotective mechanisms following cerebral I/R, but only a few studies have focused on the mechanisms associated with Glu to date. Given that Glu plays an important and complex pathophysiological role, the understanding of Glu-related mechanisms of IPostC is an interesting area of research, which we review here.

Serum Folate Correlates with Severity of Guillain-Barré Syndrome and Predicts Disease Progression.

The aim of this study was to determine the associations between serum folate level and the clinical course and severity of Guillain-Barré syndrome (GBS). We retrospectively enrolled 112 pairs of GBS patients and age- and sex-matched healthy controls with measured serum folate levels. On admission, 21 (18.9%) GBS patients had folate deficiency, of which only two were female patients. Patients with normal folate levels had a shorter disease progression than those with folate deficiency (median progression duration: 6 versus 13 days, p < 0.001). Serum folate levels on admission were correlated with progression duration and Medical Research Council (MRC) sum score in the upper limbs at nadir (r = -0.261, p = 0.005; r = -0.208, p = 0.03) but not with the duration of hospital stay or GBS disability score (p > 0.05). Logistic regression analysis revealed that normal folate levels on admission were an independent predictor of faster GBS progression, along with younger age, intact deep sensation, and a lower MRC sum score on admission. These results show that serum folate levels are correlated with the progression duration and severity of GBS. Further studies are required to confirm the potential of folate level as a biomarker for GBS prognosis.

Astrocytic gap junction inhibition by carbenoxolone enhances the protective effects of ischemic preconditioning following cerebral ischemia.

BACKGROUND: Stroke is the second leading cause of death worldwide and the most common cause of adult-acquired disability in many nations. Thus, attenuating the damage after ischemic injury and improving patient prognosis are of great importance. We have indicated that ischemic preconditioning (IP) can effectively reduce the damage of ischemia reperfusion and that inhibition of gap junctions may further reduce this damage. Although we confirmed that the function of gap junctions is closely associated with glutamate, we did not investigate the mechanism. In the present study, we aimed to clarify whether the blockade of cellular communication at gap junctions leads to significant reductions in the levels of glutamate released by astrocytes following cerebral ischemia. METHODS: To explore this hypothesis, we utilized the specific blocking agent carbenoxolone (CBX) to inhibit the opening and internalization of connexin 43 channels in an in vitro model of oxygen-glucose deprivation/re-oxygenation (OGD/R), following IP. RESULTS: OGD/R resulted in extensive astrocytic glutamate release following upregulation of hemichannel activity, thus increasing reactive oxygen species (ROS) generation and subsequent cell death. However, we observed significant increases in neuronal survival in neuron-astrocyte co-cultures that were subjected to IP prior to OGD/R. Moreover, the addition of CBX enhanced the protective effects of IP during the re-oxygenation period following OGD, by means of blocking the release of glutamate, increasing the level of the excitatory amino acid transporter 1, and downregulating glutamine expression. CONCLUSIONS: Our results suggest that combined use of IP and CBX represents a novel therapeutic strategy to attenuate damage from cerebral ischemia with minimal adverse side effects.

Roles of astrocytic connexin-43, hemichannels, and gap junctions in oxygen-glucose deprivation/reperfusion injury induced neuroinflammation and the possible regulatory mechanisms of salvianolic acid B and carbenoxolone.

BACKGROUND: Glia-mediated neuroinflammation is related to brain injury exacerbation after cerebral ischemia/reperfusion (I/R) injury. Astrocytic hemichannels or gap junctions, which were mainly formed by connexin-43, have been implicated in I/R damage. However, the exact roles of astrocytic hemichannels and gap junction in neuroinflammatory responses induced by I/R injury remain unknown. METHODS: Primary cultured astrocytes were subjected to OGD/R injury, an in vitro model of I/R injury. Salvianolic acid B (SalB) or carbenoxolone (CBX) were applied for those astrocytes. Besides, Cx43 mimetic peptides Gap19 or Gap26 were also applied during OGD/R injury; Cx43 protein levels were determined by western blot and cytoimmunofluorescene staining, hemichannel activities by Ethidium bromide uptake and ATP concentration detection, and gap junction intercellular communication (GJIC) permeability by parachute assay. Further, astrocyte-conditioned medium (ACM) was collected and incubated with microglia. Meanwhile, ATP or apyrase were applied to explore the role of ATP during OGD/R injury. Microglial activation, M1/M2 phenotypes, and M1/M2-related cytokines were detected. Also, microglia-conditioned medium (MEM) was collected and incubated with astrocytes to further investigate its influence on astrocytic hemichannel activity and GJIC permeability. Lastly, effects of ACM and MCM on neuronal viability were detected by flow cytometry. RESULTS: We found that OGD/R induced abnormally opened hemichannels with increased ATP release and EtBr uptake but reduced GJIC permeability. WB tests showed decreased astrocytic plasma membrane's Cx43, while showing an increase in cytoplasma. Treating OGD/R-injured microglia with ATP or OGD/R-ACM induced further microglial activation and secondary pro-inflammatory cytokine release, with the M1 phenotype predominating. Conversely, astrocytes incubated with OGD/R-MCM exhibited increased hemichannel opening but reduced GJIC coupling. Both SalB and CBX inhibited abnormal astrocytic hemichannel opening and ATP release and switched the activated microglial phenotype from M1 to M2, thus providing effective neuroprotection. Application of Gap19 or Gap26 showed similar results with CBX. We also found that OGD/R injury caused both plasma membrane p-Cx43(Ser265) and p-Src(Tyr416) significantly upregulated; application of SalB may be inhibiting Src kinase and attenuating Cx43 internalization. Meanwhile, CBX treatment induced obviously downregulation of p-Cx43(Ser368) and p-PKC(Ser729) protein levels in plasma membrane. CONCLUSIONS: We propose a vicious cycle exists between astrocytic hemichannel and microglial activation after OGD/R injury, which would aggravate neuroinflammatory responses and neuronal damage. Astrocytic Cx43, hemichannels, and GJIC play critical roles in OGD/R injury-induced neuroinflammatory responses; treatment differentially targeting astrocytic Cx43, hemichannels, and GJIC may provide novel avenues for therapeutics during cerebral I/R injury.

The usefulness of chief complaints to predict severity, ventilator dependence, treatment option, and short-term outcome of patients with Guillain-Barré syndrome: a retrospective study.

BACKGROUND: It remains an urgent need for early recognition of disease severity, treatment option and outcome of Guillain-Barré syndrome (GBS). The chief complaint may be quickly obtained in clinic and is one of the candidates for early predictors. However, studies on the chief complaint are still lacking in GBS. The aim of the study is to describe the components of chief complaints of GBS patients, and to explore association between chief complaints and disease severity/treatment option/outcome of GBS, so as to aid the early prediction of the disease course and to assist the clinicians to prescribe an optimal early treatment. METHODS: A total of 523 GBS patients admitted to the First Hospital of Jilin University from 2003 to 2013 were enrolled for retrospective analysis. The data of chief complaints, clinical manifestations, and treatment options, etc. were collected. The clinical severity was evaluated by the Medical Research Council sum score and the Hughes Functional Grading Scale. The prognosis at 6 month after discharge was described by modified Erasmus GBS outcome score. The clinic GBS severity evaluation scale (CGSES), a newly established model in our study, was used to explore the role of chief complaints to predict intravenous immunoglobulin (IVIg). RESULTS: The major components of the chief complaints of GBS patients were weakness, numbness, pain, cranial nerve involvement, dyspnea, ataxia and autonomic dysfunction. Chief complaint of weakness was a predictor of severe disease course and poor short-term outcome, while chief complaint of numbness and cranial nerve involvement were promising predictors. Cranial nerve involvement was the predictor of ventilator dependence. The percentages of 366 GBS patients, who need IVIg treatment at nadir with CGSES ranging from 1 to 4, were 50.00, 67.34, 80.61, and 90.67%, respectively. CONCLUSIONS: Chief complaints are clinic predictors of disease severity, ventilator dependence and short-term outcome. IVIg treatment during hospitalisation could be predicted in clinic using CGSES score.

Research and Clinical Application of Three-Dimensional Location of Amygdaloid Body.

Accurately representing the spatial location of the amygdaloid body can lay an anatomical basis for the neurosurgery operation for amputation of the amygdaloid body through lateral fissure approach. As we know, there are a number of nerve nucleuses and essential structures locating around amygdaloid body in our brain, especially optic tract. However, only few research had been done to protect these tissues or nerve nucleuses. Thus, we reconstructed the three-dimensional images of the amygdaloid body of the human brain and established a coordinate system. The morphological parameters of the amygdaloid body and the three-dimensional coordinate data were measured. The spherical coordinates (R, θ, ϕ) were constructed by calculating the azimuth angle, elevation angle, and the distance from the coordinates origin to each amygdaloid body centroid. Sixty people brain MRI images without any visible organic disease were used in our research to investigate the average level of related parameters. The authors selected a proper coordinate origin and measured the value of anteroposterior diameter, right-and-left diameter, vertical diameter of the amygdaloid body, and the distance from the optic tract to amygdaloid body. The authors also measured the three-dimensional coordinate data of each centroid of the amygdaloid body in order to provide anatomical suggestion for surgery. The authors confirmed the nearest point from the foremost edge of the brain ventricle temporal horn to the lateral fissure, then viewed it as the coordinate origin. By means of coordinate translation, the authors got various morphological parameters and the coordinate values of each centroid of the amygdaloid body. Spherical coordinates were calculated from the three-dimensional coordinate values. The distances between the different layers of the amygdaloid body and the optic tract were also measured. The reconstruction of the three-dimensional coordinates of amygdaloid body is part of the digital engineering of the human body. The measurement of the parameters provides an important theoretical basis for the clinical amygdaloid body destruction surgery. Finally, the authors get conclusions as follows. There are no significant differences in the measured values of r1, r2, and r3 between the upper and lower diameters, the left and right diameters, the anteroposterior diameter of the amygdaloid body. The measured values of men and women are not statistically significant (P > 0.05). Spherical coordinates (R, θ, ϕ) calculated from the three-dimensional coordinate values and values from different sexes of the amygdaloid body are not statistically significant, either (P > 0.05). The distance between the different levels of the amygdaloid body and the optic tract (h1, h2, h3, h4, h5, h6, and h7) are not statistically significant (P > 0.05).