Abstract Background Most of the knowledge on Mycoplasma pneumoniae encephalitis (MPE) in children is based on case reports or small case series.This study aimed to describe the clinical features, the efficacy of azithromycin with or without immunomodulatory therapy ,and prognostic factors of MPE . Methods The Medical data of eighty-seven MPE patients from three medical centers in southwestern China over a 7-years period were reviewed. Results MPE was noted in children of all ages except for neonates.The most common neurological manifestations include consciousness disturbance(90%) and headache(87.4%),the most common extra-neurological presentations include fever (96.5%)and respiratory system involvement(94.3%) ,multi-system involvement(98.2%) and elevated C-reactive protein(CRP) (90.8%)were also prominent. M. pneumoniae detection in CSF was less than in blood and respiratory tract secretions.Azithromycin with intravenous immunoglobulin (IVIG) or/and corticosteroids treatment can shorten the hospitalization duration and length of clinical improvement. Multivariate analysis revealed that onset during teenage years and high lactate dehydrogenase (LDH) and CSF protein levels were identified as independent prognostic factors for poor outcome. Conclusions In children having acute encephalitis with multi-system involvement, especially in those with respiratory tract manifestations, accompanied with prominently elevated CRP,M. pneumoniae should be given preference.Higher age,marked CSF protein and blood LDH were correlated with unfavorable outcomes. Multiplicity mechanisms ,especially immune-mediated inflammation involved in the pathogenesis. Immunomodulating therapies should be recommended regardless of the duration of prodromal period.
Epilepsy can be defined as a dysfunction of the brain network, and each type of epilepsy involves different brain-network changes that are implicated differently in the control and propagation of interictal or ictal discharges. Gaining more detailed information on brain network alterations can help us to further understand the mechanisms of epilepsy and pave the way for brain network-based precise therapeutic approaches in clinical practice. An increasing number of advanced neuroimaging techniques and electrophysiological techniques such as diffusion tensor imaging-based fiber tractography, diffusion kurtosis imaging-based fiber tractography, fiber ball imaging-based tractography, electroencephalography, functional magnetic resonance imaging, magnetoencephalography, positron emission tomography, molecular imaging, and functional ultrasound imaging have been extensively used to delineate epileptic networks. In this review, we summarize the relevant neuroimaging and neuroelectrophysiological techniques for assessing structural and functional brain networks in patients with epilepsy, and extensively analyze the imaging mechanisms, advantages, limitations, and clinical application ranges of each technique. A greater focus on emerging advanced technologies, new data analysis software, a combination of multiple techniques, and the construction of personalized virtual epilepsy models can provide a theoretical basis to better understand the brain network mechanisms of epilepsy and make surgical decisions.
The method for the determination of Cr(VI) and Cr(Ⅲ) in the passivation film of chromate was studied.Thus humic acid resin powders were prepared by cross-linking of humic acid in the presence of phenolic resin.The adsorption characteristics and separation and concentration of Cr(VI) and Cr(Ⅲ) by the humic acid resin were investigated by means of flame atomic absorption spectrometry(FAAS).The results showed that Cr(Ⅵ) could be quantitatively adsorbed by the humic acid resin at a pH value below 1,when Cr(Ⅲ) could not be adsorbed.At a pH value above 5,Cr(Ⅲ) could be adsorbed,but Cr(Ⅵ) could not be adsorbed.Therefore,it was feasible to separate Cr(Ⅵ) and Cr(Ⅲ) by adjusting the pH value of the medium.Namely,Cr(Ⅵ) and Cr(Ⅲ) adsorbed on the humic acid resin could be completely eluted using 0.5 mol/L NaOH and 1 mol/L HCl solution,respectively.Then Cr(Ⅵ) and Cr(Ⅲ) could be determined using FAAS.The corresponding newly established method could be satisfactorily applied for the determination of Cr(Ⅵ) and Cr(Ⅲ) in the passivation film of chromate.
Epilepsy is a common disease of the nervous system. Autophagy is a degradation process involved in epilepsy, and in turn, seizures can activate autophagy. Beclin1 plays a critical role in autophagy and participates in numerous physiological and pathological processes. However, the mechanism underlying the effect of Beclin1 on epilepsy remains unclear. In this study, we detected increased expression of Beclin1 in brain tissues from patients with temporal lobe epilepsy (TLE). Heterozygous disruption of beclin1 decreased susceptibility to epilepsy and suppressed seizure activity in two mouse epilepsy models. We further illustrated for the first time that heterozygous disruption of beclin1 suppresses excitatory synaptic transmission, which may be caused by a decreased dendritic spine density. These findings suggest for the first time that the regulation of Beclin1 may serve as a strategy for antiepileptic therapy. In addition, Beclin1 participates in synaptic transmission, and the development of dendritic spines may be a biological function of Beclin1 independent of its role in autophagy.
Objective: To evaluate the safety and efficacy of endovascular thrombectomy (EVT) in acute anterior circulation large vessel occlusive stroke (ALVOS) and explore the related influencing factors for prognoses in patients with low Alberta Stroke Program Early Computed Tomography Score (ASPECT). Methods: Patients with acute ALVOS who underwent EVT in Yijishan Hospital of Wannan Medical College from January 2019 to June 2022 were sequentially enrolled. (1) Patients were divided into a low ASPECT group (0-5) and a non-low ASPECT group (6-10), and the differences between the two groups were compared with respect to incidence of perioperative complications and good prognosis rate [modified Rankin scale (mRS) score≤2] 90 days after onset. (2) According to the prognoses 90 days after onset, the low ASPECT group was divided into the good prognosis (mRS score≤2) and poor prognosis (mRS score>2) subgroup. Univariate analysis and multivariate logistic regression analysis were used to investigate the independent risk factors for prognoses of the low ASPECT patients after EVT. Results: A total of 582 patients [age 26-94(69±11) years, 345 male patients (59.3%)] were enrolled for analysis. The baseline ASPECT score was 8 (7, 10), and the baseline NIHSS score was 14 (11, 18). Among them, 102 (17.5%) patients were in the low ASPECT score group and 480 (82.5%) patients were in the non-low ASPECT score group. In the total cohort, patients in the low ASPECT score group had a higher incidence of symptomatic intracranial hemorrhage, lower 90-day good prognosis rate, and higher 90-day mortality rate. Further, propensity score matching statistical analysis showed that patients in the low ASPECT score group had a significantly higher incidence of malignant brain edema after EVT treatment (40.0% vs. 17.6%, χ2=9.13, P=0.003), and a significantly lower 90-day good prognosis rate (24.7% vs. 41.6%, χ2=4.96, P=0.026), but there was no significant difference in the incidence of symptomatic intracranial hemorrhage and 90-day mortality between the two groups (40.3% vs. 26.0%, χ2=3.55, P=0.060). Among 102 patients with low ASPECT score, 22 (21.6%) patients had good prognosis and 80 (78.4%) had poor prognosis. Multivariate logistic regression analysis showed that history of atrial fibrillation (OR=4.478, 95%CI 1.186-16.913, P=0.027) was an independent risk factor for poor prognosis of EVT in patients with low ASPECT score, while good collateral circulation (grade 2 vs. grade 0: OR=0.206, 95%CI 0.051-0.842, P=0.028) was a protective factor for good prognosis of EVT in patients with low ASPECT score. Conclusions: Although the 90-day good prognosis rate of EVT treatment for patients with low ASPECT score was lower than that of the non-low ASPECT group, 21.6% patients still benefitted from EVT treatment, especially patients with non-atrial fibrillation and good collateral circulation. Future studies involving more patients are needed to validate our observations.目的: 评估低基线Alberta卒中计划早期CT(ASPECT)评分急性大血管闭塞性卒中患者早期血管内治疗(EVT)的安全性及有效性,并探讨影响该类患者预后的相关因素。 方法: 回顾性收集皖南医学院第一附属医院(弋矶山医院)卒中中心2019年1月至2022年6月收治的行EVT治疗的前循环急性大血管闭塞性卒中患者582例纳入分析,年龄26~94(69±11)岁,男性患者345例(59.3%)。(1)根据基线ASPECT评分将患者分为低评分组(0~5分)与非低评分组(6~10分),比较2组间围手术期并发症发生率、90 d预后良好率[改良Rankin量表(mRS)评分≤2分]及病死率的差异。(2)根据90 d预后情况将低评分组患者分为预后良好亚组(mRS评分≤2分)与预后不良亚组(mRS评分>2分),采用单因素分析及多因素logistic回归分析探讨影响低ASPECT评分患者EVT治疗预后的独立危险因素。 结果: 基线ASPECT评分为8(7,10)分,基线美国国立卫生研究院卒中量表(NIHSS)评分为14(11,18)分;其中低ASPECT评分组患者102例(17.5%),非低ASPECT评分组患者480例(82.5%)。总体人群中,低ASPECT评分组患者中症状性颅内出血发生率更高、90 d良好预后率更低、90 d病死率更高,进一步对两组患者的基线资料进行倾向性评分匹配(1∶1)后统计分析显示,低ASPECT评分组患者经EVT治疗后恶性脑水肿发生率明显高于非低ASPECT评分组(40.0% 比 17.6%,χ2=9.13,P=0.003)、90 d预后良好率明显低于非低ASPECT评分组(24.7% 比 41.6%,χ2=4.96,P=0.026),差异有统计学意义,但2组患者间症状性颅内出血发生率(11.8% 比 9.2%,χ2=0.28,P=0.597)、90 d病死率(40.3% 比 26.0%,χ2=3.55,P=0.060)差异均无统计学意义。102例低ASPECT评分组患者中,预后良好患者22例(21.6%),预后不良患者80例(78.4%)。多因素logistic回归分析显示,既往心房颤动病史(OR=4.478,95%CI 1.186~16.913,P=0.027)是低ASPECT评分组患者EVT治疗预后不良的独立危险因素,而良好的侧支循环(2级比0级:OR=0.206,95%CI 0.051~0.842,P=0.028)是低ASPECT评分组患者EVT治疗预后良好的保护因素。 结论: 低ASPECT评分患者行EVT治疗尽管90 d良好预后率低于非低评分组,但仍有21.6%的患者获益,尤其是对具有良好侧支循环的非房颤患者,结论仍需进一步循证医学证据证实。.
Abstract To investigate the clinical characteristics of febrile infection‐related epilepsy syndrome (FIRES). We used trajectory analysis and logistic regression analysis to investigate the clinical characteristics and prognostic risk factors respectively. Twenty‐seven patients (16 males) were included. The median age of onset was 7 (IQR: 4–9) years. Routine cerebrospinal fluid (CSF) examination was normal. Electroencephalogram (EEG) showed frequent microseizures and electroseizures in all patients. Eight patients had claustrum signs in the acute phase. Anesthetics and anti‐seizure medications (ASM) were used in all patients. All patients received immunotherapy, including plasma exchange ( n = 4), immunoglobulin ( n = 26), and corticosteroids ( n = 19). Trajectory diagrams of seizure showed 6 patients had bimodal disease course. Besides, we found there may be a linear relationship between body temperature and convulsion frequency ( R 2 = 0.25). The median Glasgow outcome scale (GOS) was 3 (IQR: 1–4). Nine deaths occurred, including abandonment of treatment ( n = 3), hemodynamic instability ( n = 3), brain hernia ( n = 2), and brain hernia with hemodynamic instability ( n = 1). Seizure onset combined with fever ( p = 0.003), periodic discharge ( p = 0.002), and non‐ketogenic diet (non‐KD) ( p = 0.005) were independent risk factors for death. The KD group ( n = 10) had lower mortality ( p = 0.009), lower convulsion frequency at latest follow‐up ( p < 0.001), less ASM ( p = 0.002), and higher GOS ( p < 0.001) than non‐KD group ( n = 17). Therefore, some FIRES patients may have bimodal disease course. There may be a linear relationship between body temperature and convulsion frequency. Seizure onset combined with fever, periodic discharge and KD may affect the prognosis.
Abstract Spindle waves occur during the early stage of slow wave sleep and are thought to arise in the thalamic reticular nucleus (TRN), causing inhibitory postsynaptic potential spindle-like oscillations in the dorsal thalamus that are propagated to the cortex. We have found that thalamocortical neurons exhibit membrane oscillations that have spindle frequencies, consist of excitatory postsynaptic potentials, and co-occur with electroencephalographic spindles. TRN lesioning prolonged oscillations in the medial geniculate body (MGB) and auditory cortex (AC). Injection of GABA~A~ antagonist into the MGB decreased oscillation frequency, while injection of GABA~B~ antagonist increased spindle oscillations in the MGB and cortex. Thus, spindles originate in the dorsal thalamus and TRN inhibitory inputs modulate this process, with fast inhibition facilitating the internal frequency and slow inhibition limiting spindle occurrence.
Abstract Background Previous studies have shown a role of mitochondrial DNA (MtDNA) in innate immunity. However, the specific role of MtDNA in chronic kidney disease (CKD)-related cardiovascular disease (CVD) remains elusive. This study was designed to investigate the potential relationship between circulating MtDNA and CVD in maintenance hemodialysis (MHD) patients, and to examine the damaging effect of exogenous MtDNA on cardiac microvascular endothelial cells (CMECs) in the uremic milieu. Methods Forty-two MHD patients and 36 health controls were enrolled in this study. Plasma cell-free MtDNA was detected by TaqMan-based qPCR assay. The CVD risk markers including high-sensitive C-reactive protein (Hs-CRP), monocyte chemoattractant protein-1 (MCP-1), fibrinogen, and erythrocyte sedimentation rate (ESR) were measured by using standard assays. The ten-year cardiovascular risk was assessed using the framingham risk score (FRS). Dialysis systems in MHD patients were used to evaluate the effect of different dialysis modes on the clearance of circulating MtDNA. In vitro study, human cardiac microvascular endothelial cells (HCMECs) were incubated with normal or uremic serum with or without exogenous MtDNA stimulation. Intracellular toll-like receptor 9 (TLR9), adhesion molecule 1 (ICAM-1), MCP-1 and tumor necrosis factor-α (TNF-α) mRNA levels and cytosolic MtDNA contents were detected by qPCR. Results Plasma MtDNA was significantly elevated in patients with MHD relative to healthy controls. The MHD patients were subsequently classified into two groups based on the median value of MtDNA. In stratified analyses, the levels of Hs-CRP and MCP-l, and FRS in the high plasma MtDNA group were higher than those in the low plasma MtDNA group. In vitro study, exogenous MtDNA aggravated uremic serum-induced upregulation of ICAM-1 and TNF-α in HCMECs. Also, the addition of MtDNA to the medium resulted in increased cytosolic MtDNA amounts and TLR9 mRNA levels in uremic serum-treated cells. Single routine hemodialysis and hemodiafiltration could partially reduce plasma MtDNA in MHD patients. These two methods seem similar in terms of MtDNA clearance. Conclusions We concluded that MtDNA released into the circulation under the uremic toxin environment may has a detrimental effect on cardiovascular system through aggravating microvascular inflammation, and that reducing circulating MtDNA might be a future therapeutic strategy for the prevention of MHD-related CVD.