Weak-Interaction Environment in a Composite Electrolyte Enabling Ultralong-Cycling High-Voltage Solid-State Lithium Batteries.

Poly(vinylidene fluoride) (PVDF)-based solid electrolytes with a Li salt-polymer-little residual solvent configuration are promising candidates for solid-state batteries. Herein, we clarify the microstructure of PVDF-based composite electrolyte at the atomic level and demonstrate that the Li+-interaction environment determines both interfacial stability and ion-transport capability. The polymer works as a "solid diluent" and the filler realizes a uniform solvent distribution. We propose a universal strategy of constructing a weak-interaction environment by replacing the conventional N,N-dimethylformamide (DMF) solvent with the designed 2,2,2-trifluoroacetamide (TFA). The lower Li+ binding energy of TFA forms abundant aggregates to generate inorganic-rich interphases for interfacial compatibility. The weaker interactions of TFA with PVDF and filler achieve high ionic conductivity (7.0 × 10-4 S cm-1) of the electrolyte. The solid-state Li||LiNi0.8Co0.1Mn0.1O2 cells stably cycle 4900 and 3000 times with cutoff voltages of 4.3 and 4.5 V, respectively, as well as deliver superior stability at -20 to 45 °C and a high energy density of 300 Wh kg-1 in pouch cells.

Efficacy and safety of low- and ultralow-dose rituximab in neuromyelitis optica spectrum disorder.

BACKGROUND: Rituximab effectively targets B cells and reduces relapses in neuromyelitis optica spectrum disorder (NMOSD). But the ideal dosage and treatment intervals remain unanswered. We aimed to assess the efficacy and safety of low and ultralow-dose rituximab in NMOSD. METHODS: We conducted a retrospective analysis of NMOSD patients treated with rituximab at two Chinese tertiary hospitals. Patients received either a low-dose regimen (500 mg reinfusion every 6 months) or an ultralow-dose regimen: 100 to 300 mg rituximab based on CD19+B cells (100 mg for 1-1.5% of peripheral blood mononuclear cells, 200 mg for 1.5-5%, and 300 mg for over 5%). RESULTS: We analyzed data from 136 patients (41 in the low-dose group, 95 in the ultralow-dose group) with median follow-up durations of 43 and 34.2 months, respectively. Both groups exhibited similar sex distribution, age at disease onset, annual relapse rate, and baseline disease duration. Survival analysis showed that ultralow-dose rituximab was noninferior to low-dose rituximab in preventing relapses. Infusion reactions occurred in 20 of 173 (11.6%) low-dose treatments and 9 of 533 (1.7%) ultralow-dose treatments. B-cell re-emergence was observed in 137 of 236 (58.1%) monitors in the low-dose group and 367 of 1136 (32.3%) monitors in the ultralow-dose group. CONCLUSION: Ultralow dose rituximab was noninferior to low-dose rituximab in preventing NMOSD relapses. A randomized controlled trial is essential to validate these findings.

Dielectric Filler-Induced Hybrid Interphase Enabling Robust Solid-State Li Metal Batteries at High Areal Capacity.

The fillers in composite solid-state electrolyte are mainly responsible for the enhancement of the conduction of Li ions but barely regulate the formation of solid electrolyte interphase (SEI). Herein, a unique filler of dielectric NaNbO3 for the poly(vinylidene fluoride) (PVDF)-based polymer electrolyte, which is subjected to the exchange of Li+ and Na+ during cycling, is reported and the substituted Na+ is engaged in the construction of a fluorinated Li/Na hybrid SEI with high Young's modulus, facilitating the fast transport of Li+ at the interface at a high areal capacity and suppressing the Li dendrite growth. The dielectric NaNbO3 also induces the generation of high-dielectric ß phase of PVDF to promote the dissociation of Li salt. The Li/Li symmetrical cell exhibits a long-term dendrite-free cycling over 600 h at a high areal capacity of 3 mA h cm-2. The LiNi0.8Mn0.1Co0.1O2/Li solid-state cells with NaNbO3 stably cycle 2200 times at 2 C and that paired with high-loading cathode (10 mg cm-2) can stably cycle for 150 times and exhibit excellent performances at -20 °C. This work provides a novel design principle of fillers undertaking interfacial engineering in composite solid-state electrolytes for developing the safe and stable solid-state lithium metal battery.

Palatal myoclonus and hypertrophic olivary degeneration following wernekinck commissure syndrome: a case report.

BACKGROUND: Hypertrophic olivary degeneration (HOD), a rare form of transsynaptic degeneration, is secondary to dentato-rubro-olivary pathway injuries in some cases. We describe a unique case of an HOD patient who presented with palatal myoclonus secondary to Wernekinck commissure syndrome caused by a rare bilateral "heart-shaped" infarct lesion in the midbrain. CASE PRESENTATION: A 49-year-old man presented with progressive gait instability in the past 7 months. The patient had a history of posterior circulation ischemic stroke presenting with diplopia, slurred speech, and difficulty in swallowing and walking 3 years prior to admission. The symptoms improved after treatment. The feeling of imbalance appeared and was aggravated gradually in the past 7 months. Neurological examination demonstrated dysarthria, horizontal nystagmus, bilateral cerebellar ataxia, and 2-3 Hz rhythmic contractions of the soft palate and upper larynx. Magnetic resonance imaging (MRI) of the brain performed 3 years prior to this admission showed an acute midline lesion in the midbrain exhibiting a remarkable "heart appearance" on diffusion weighted imaging. MRI after this admission revealed T2 and FLAIR hyperintensity with hypertrophy of the bilateral inferior olivary nucleus. We considered a diagnosis of HOD resulting from a midbrain heart-shaped infarction, which caused Wernekinck commissure syndrome 3 years prior to admission and later HOD. Adamantanamine and B vitamins were administered for neurotrophic treatment. Rehabilitation training was also performed. One year later, the symptoms of this patient were neither improved nor aggravated. CONCLUSION: This case report suggests that patients with a history of midbrain injury, especially Wernekinck commissure injury, should be alert to the possibility of delayed bilateral HOD when new symptoms occur or original symptoms are aggravated.

Ultrathin and Robust Composite Electrolyte for Stable Solid-State Lithium Metal Batteries.

Solid-state polymer electrolytes (SPEs) are considered as one of the most promising candidates for the next-generation lithium metal batteries (LMBs). However, the large thickness and severe interfacial side reactions with electrodes seriously restrict the application of SPEs. Herein, we developed an ultrathin and robust poly(vinylidene fluoride) (PVDF)-based composite polymer electrolyte (PPSE) by introducing polyethylene (PE) separators and SiO2 nanoparticles with rich silicon hydroxyl (Si-OH) groups (nano-SiO2). The thickness of the PPSE is only 20 µm but possesses a quite high mechanical strength of 64 MPa. The introduction of nano-SiO2 fillers can tightly anchor the essential N,N-dimethylformamide (DMF) to reinforce the ion-transport ability of PVDF and suppress the side reactions of DMF with Li metal, which can significantly enhance the electrochemical stability of the PPSE. Meanwhile, the Si-OH groups on the surface of nano-SiO2 as a Lewis acid promote the dissociation of the lithium bis(fluorosulfonyl)imide (LiFSI) and immobilize the FSI- anions, achieving a high lithium transference number (0.59) and an ideal ionic conductivity (4.81 × 10-4 S cm-1) for the PPSE. The assembled Li/PPSE/Li battery can stably cycle for a record of 11,000 h, and the LiNi0.8Co0.1Mn0.1O2/PPSE/Li battery presents an initial specific capacity of 173.3 mA h g-1 at 0.5 C, which can stably cycle 300 times. This work provides a new strategy for designing composite solid-state electrolytes with high mechanical strength and ionic conductivity by modulating their framework.

A prospective study on tryptophan immunoadsorption in AQP4 antibody-positive neuromyelitis optica spectrum disorders.

INTRODUCTION: Neuromyelitis optica spectrum disorders (NMOSD) is a rare inflammatory demyelinating disease of the central nervous system. NMOSD pathogenesis is mainly mediated by antibodies directed against aquaporin4 (AQP4 antibody). Immunoadsorption (IA) could specifically remove pathogenic antibody to alleviate the disease. Until now, prospective studies concerning the efficacy of IA on NMOSD are scarce. This study aims to prospectively evaluate the efficacy and safety of IA in the treatment of NMOSD. PATIENTS AND METHODS: We included patients with AQP4 antibody-positive NMOSD who were hospitalized from September 2019 to September 2020, with no significant improvement in symptoms after 1 week of high-dose intravenous steroid therapy. Tryptophan IA therapy was initiated with five sessions on alternate days. Expanded Disability Status Scale (EDSS), visual acuity, and laboratory values were measured before and after IA, with a follow-up of 6 months. Spinal magnetic resonance imaging (MRI) characteristics were collected. Related side effects were recorded. RESULTS: Seven patients were enrolled in the present study. After five IA, the patients' EDSS decreased from 5.71 ± 2.04 to 4.64 ± 2.29, P = .006. The visual acuity of the three visually impaired patients was improved. AQP4-IgG decreased significantly from 80.00 (interquartile range [IQR], 21.00-80.00) (U/mL) to 9.72 (IQR, 5.21-55.57) (U/mL) (P = .018). MRI of the spinal cord showed the scope of the myelopathy was narrowed and no significant enhancement was observed on postcontrast T1-weighted image at 90 days after treatment. Only one patient had transient hypotension. CONCLUSIONS: Tryptophan IA therapy effectively and safely improved neurological function and visual acuity, and reduced the AQP4 antibody concentration in patients with NMOSD.

Soluble TREM2 is a potential biomarker for the severity of primary angiitis of the CNS.

Background: Primary angiitis of the central nervous system (PACNS) is a severe inflammatory disease, and soluble triggering receptor expressed on myeloid cells 2 (sTREM2) has been reported to be associated with inflammation of the CNS. However, the role of sTREM2 in PACNS remains unknown. Methods: We obtained serum and cerebrospinal fluid (CSF) samples from 18 patients diagnosed with PACNS, as well as 14 patients diagnosed with other neurological disorders with no evidence of inflammation. sTREM2 concentrations in the samples were detected by enzyme-linked immunosorbent assay. And routine CSF measurements of PACNS patients were analysed, including number of White Blood Cells (WBC), protein, Immunoglobulin G (IgG) index and CSF/serum quotients. Levels of inflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-6, IL-8, IL-1ß, and complement C4, also were tested. The modified Rankin scale (mRS), National Institutes of Health Stroke Scale (NIHSS), and activities of daily living (ADL) scores were obtained as indicators of disease severity. In PACNS patients, cerebral lesion volume was evaluated by magnetic resonance imaging. Results: sTREM2 levels in serum and CSF were significantly elevated in PACNS patients and significantly associated with the mRS, NIHSS and ADL scores as well as inflammatory cytokine levels. Additionally, positive correlations were observed between the cerebral lesion volume and the sTREM2 levels in both blood and CSF. Higher sTREM2 levels in either the blood or CSF seemed to predict a good prognosis in PACNS patients. Conclusion: Our results indicate an association between serum and CSF sTREM2 levels and the severity of neurological damage. Thus, sTREM2 represents a potential biomarker for monitoring disease and potentially predicting the prognosis of PACNS patients.

Thymic Involution and Altered Naive CD4 T Cell Homeostasis in Neuromyelitis Optica Spectrum Disorder.

Circulating T helper cells with a type 17-polarized phenotype (TH17) and expansion of aquaporin-4 (AQP4)-specific T cells are frequently observed in patients with neuromyelitis optica spectrum disorder (NMOSD). However, naive T cell populations, which give rise to T helper cells, and the primary site of T cell maturation, namely the thymus, have not been studied in these patients. Here, we report the alterations of naive CD4 T cell homeostasis and the changes in thymic characteristics in NMOSD patients. Flow cytometry was performed to investigate the naive CD4+ T cell subpopulations in 44 NMOSD patients and 21 healthy controls (HC). On immunological evaluation, NMOSD patients exhibited increased counts of CD31+thymic naive CD4+ T cells and CD31-cental naive CD4+ T cells along with significantly higher fraction and absolute counts of peripheral blood CD45RA+ CD62L+ naive CD4+ T cells. Chest computed tomography (CT) images of 60 NMOSD patients and 65 HCs were retrospectively reviewed to characterize the thymus in NMOSD. Thymus gland of NMOSD patients exhibited unique morphological characteristics with respect to size, shape, and density. NMOSD patients showed exacerbated age-dependent thymus involution than HC, which showed a significant association with disease duration. These findings broaden our understanding of the immunological mechanisms that drive severe disease in NMOSD.

NF-κB 1-induced LINC00665 regulates inflammation and apoptosis of neurons caused by spinal cord injury by targeting miR-34a-5p.

Background: Spinal cord injury (SCI) has high disability rate and low cure rate, which frustrates the patients and brings a heavy burden to their families. This study aimed to explore whether NF-κB1 could induce the expression of LINC00665 and form a feedback loop with miR-34a-5p to regulate inflammation and apoptosis of neurons. Results: Basso, Beattie, and Bresnahan (BBB) scoring was decreased, damage for spinal cord tissue was aggravated and neuron number was decreased in SCI rats. The levels of TNF-α, IL-1ß and IL-6 in serum and the expression of LINC00665 and NF-κB1 in spinal cord tissues were all increased in SCI rats. After LPS induction, PC12 cell viability was decreased. The expression of LINC00665 and NF-κB1 in LPS-induced PC12 cells was increased, which was partially reversed by BAY11-7082 (NF-κB inhibitor). Inhibition of LINC00665 improved cell viability, suppressed apoptosis and inflammation and down-regulated the NF-κB1 expression in LPS-induced PC12 cells. Furthermore, miR-34a-5p expression was decreased in LPS-induced PC12 cells, which could be promoted by inhibition of LINC00665. miR-34a-5p inhibitor restrained the effect of inhibition of LINC00665 on NF-κB1 expression in LPS-induced PC12 cells. Conclusion: inhibition of LINC00665 improved cell viability, suppressed apoptosis and inflammation in LPS-induced PC12 cells, and the NF-κB1/LINC00665/miR-34a-5ploop might be a useful therapeutic target in SCI treatment.

TRPV1, Targeted by miR-338-3p, Induces Neuropathic Pain by Interacting with NECAB2.

A variety of studies have proposed that transient receptor potential vanilloid 1 (TRPV1) is involved in the progression of multiple diseases, including neuropathic pain. Although increased expression of TRPV1 in chronic constriction injury was described earlier, the underlying regulatory mechanisms of TRPV1 in neuropathic pain remain largely unknown. In our study, we constructed a chronic constriction injury (CCI) rat model to deeply analyze the mechanisms underlying TRPV1. RT-qPCR-indicated TRPV1 mRNA and protein expression were extremely upregulated in CCI rat dorsal spinal cord tissues. Then, TRPV1 was corroborated to interact with N-terminal EF-hand Ca2+-binding protein 2 (NECAB2). The mRNA and protein levels of NECAB2 were increased in CCI tissues. Moreover, TRPV1 and NECAB2 together regulated nociceptive procession-associated protein metabotropic glutamate receptor 5 (mGluR5), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and Ca2+ in isolated microglia of CCI rats. Moreover, TRPV1 upregulation apparently increased mechanical allodynia and thermal hyperalgesia as well as the expression of inflammation-associated genes (COX-2, TNF-α, and IL-6). In addition, downregulation of NECAB2 significantly decreased mechanical allodynia and thermal hyperalgesia as well as the expression of COX-2, TNF-α, and IL-6. Furthermore, TRPV1 was confirmed to be a downstream target of miR-338-3p. TRPV1 overexpression abolished the inhibitory effect by miR-338-3p elevation on neuropathic pain development. In summary, this study proved TRPV1, targeted by miR-338-3p, induced neuropathic pain by interacting with NECAB2, which provides a potential therapeutic target for neuropathic pain treatment.

Case Report: Innate Immune System Challenge Unleashes Paraneoplastic Neurological Autoimmunity.

Paraneoplastic autoimmune neurological disorders reflect tumor-initiated immune responses against onconeural antigens. Symptoms and signs can affect the central and/or peripheral nervous systems, neuromuscular junction or muscle, and typically evolve subacutely before an underlying neoplasm is discovered. We describe four patients whose neurological symptoms were precipitated by potent innate immune system challenges: bladder instillation of BCG, tick bite and an "alternative cancer therapy" with bacterial extracts and TNF-α. We hypothesize that a tumor-initiated autoimmune response (evidenced by autoantibody profiles), pre-dating the immune system challenge, was unmasked or amplified in these patients by cytokines released systemically from innate immune cells activated by microbial pathogen-associated molecular patterns (PAMPs). The resultant upregulation of cognate onconeural peptides as MHC1 protein complexes on neural cell surfaces would render those cells susceptible to killing by CD8+ T cells, thus precipitating the patient's neurological symptoms.

Cortical Thinning and Ventricle Enlargement in Neuromyelitis Optica Spectrum Disorders.

Background: In neuromyelitis optica spectrum disorders (NMOSDs), inflammation is not the sole driver of accumulation of disability; neurodegeneration is another important pathological process. We aim to explore different patterns of cortical atrophy and ventricular enlargement in NMOSD. Methods: We retrospectively analyzed a cohort of 230 subjects, comprising 55 healthy controls (HCs), 85 multiple sclerosis (MS), and 90 NMOSD patients from Tianjin Medical University General Hospital and Beijing Tiantan Hospital. Different compartments of the brain (total gray, cortex, subcortex gray, and ventricle volume) were evaluated with the FreeSurfer. Multiple linear regressions were adopted to explore associations between cortex volume and predict factors. Results: Compared with HCs, NMOSD, and MS displayed an enlarged lateral and third ventricle (p < 0.001), whereas expansion of the fourth ventricle was observed in MS rather than NMOSD (p = 0.321). MS and NMOSD patients exhibited cortical thinning in comparison with HCs. However, pronounced cortical atrophy were only significant in pre-cuneus, parahippocampal, and lateral occipital lobe between MS and NMOSD. Patients with NMOSD had decreased local gyrification index in orbitofrontal and pre-cuneus lobe, and reduced pial surface area. Linear regression analysis revealed cortex volume were predicated by advanced age (standardized ß = -0.404, p = 0.001) as well as prolonged disease history (standardized ß = -0.311, p = 0.006). Conclusion: NMOSD exhibited global cortex atrophy with enlarged lateral and third ventricles. Moreover, cortex volume is associated with age and disease duration.

Anti-NMDA receptor encephalitis concomitant with myelin oligodendrocyte glycoprotein antibody diseases: A retrospective observational study.

Anti-N-methyl-D-aspartate receptor encephalitis (NMDARe) can coexist with myelin oligodendrocyte glycoprotein antibody (MOG-ab) disease.To characterize MOG-ab disease during NMDARe, we analyzed all the patients with MOG-ab disease and NMDARe from our hospital from December 2018 to December 2019 and data from a systematical review of previously published reports. Details of the patients identified were summarized and literature was reviewed.Four of thirty (14.2%) patients with anti-NMDARe had overlapping MOG-ab disease in our department. Analyze together with previously reported cases. Thirty-two NMDARe patients had overlapping MOG-ab disease. The onset age ranged from 3 to 48 years. Twenty-four patients (74%) developed abnormal behavior or cognitive dysfunction during the episodes of anti-NMDARe. None of these patients had tumors. 84% (27/32) patients received high doses of steroids as first-line immunotherapy and 28% (9/32) received mycophenolate mofetil (MMF) to prevent relapse. Twenty-six of twenty-seven (96%) had a good outcome.Steroids are the most common first-line immunotherapies in NMDARe overlapping MOG-ab disease. Most of the NMDARe patients overlapping MOG-ab disease have a good prognosis.

Cytokines and Tissue Damage Biomarkers in First-Onset Neuromyelitis Optica Spectrum Disorders: Significance of Interleukin-6.

OBJECTIVE: We investigated the contribution of several cytokines in the pathogenesis of first-onset neuromyelitis optica spectrum disorder (NMOSD) and determined the differences between aquaporin 4 immunoglobulin G (AQP4-IgG)-positive and AQP4-IgG-negative subtypes. METHODS: We enrolled 18 NMOSD (10 AQP4-IgG-positive and 8 AQP4-IgG-negative) and 8 multiple sclerosis (MS) patients, whose serum and cerebrospinal fluid (CSF) samples were collected during the acute phase of the first onset before immunotherapy. Fifteen patients with other noninflammatory neurological diseases (OND) were also included. The serum and CSF levels of interleukin (IL)-6, IL-10, IL-17, IL-21, IL-23, transforming growth factor (TGF)-ß1 and the CSF levels of 3 biomarkers of axonal loss and astrocytic damage were measured using the human cytokine multiplex assay or ELISA. RESULTS: Serum levels of IL-10 and TGF-ß1 and CSF levels of IL-6, IL-10, and TGF-ß1 were significantly increased in first-onset NMOSD compared to in OND patients. In a subgroup analysis, the CSF levels of IL-6, neurofilament light protein (NFL), S100B, and glial fibrillary acidic protein (GFAP) were significantly more elevated in the AQP4-IgG-positive patients than in the AQP4-IgG-negative NMOSD patients. Correlations were found between the CSF cytokines and tissue damage biomarkers and the clinical findings in NMOSD patients. Notably, the CSF IL-6 level had the strongest correlation with the tissue damage biomarkers and it also correlated with CSF white blood cell (WBC) count. CONCLUSIONS: IL-6 plays a role in the pathogenetic process of NMOSD, especially in the AQP4-IgG-positive subtype. Distinct pathogenesis exists between AQP4-IgG-positive and AQP4-IgG-negative NMOSD in the initial phase of the disease.

Predictors of neurological deterioration during hospitalization: results from the Chinese Intracranial Atherosclerosis (CICAS) Study.

OBJECTIVES: Neurological deterioration (ND) after ischaemic stroke has been indicated as an independent risk factor for poor outcome. Previous studies have focussed on ND within the first few days after symptom onset, but many patients are likely to experience deterioration outside of this time frame. We aimed to investigate the predictors of ND during hospitalisation. METHODS: Data were obtained from the Chinese Intracranial Atherosclerosis (CICAS) Study, and patients who were diagnosed with ischaemic stroke and arrived at the hospital within 72  hours after symptom onset were included in the present study. Neurological deterioration was defined as an increase in the National Institutes of Health Stroke Scale (NIHSS) score of ≥ 2 points at discharge compared with admission. MR angiography (MRA) and duplex colour Doppler ultrasound were used to document the presence of intracranial or extracranial artery stenosis. Intracranial artery stenosis was defined as a reduction in the artery diameter of ≥ 50% on MRA. Multivariate analyses were conducted to determine the potential predictors of ND during hospitalisation. RESULTS: Of the 1996 patients included in this study, 84 (4.21%) developed ND during hospitalisation. Compared with non-ND patients, ND patients showed higher rates of pneumonia (25.0 vs 9.5%, P < 0.001), urinary infection (7.1 vs 1.2%, P < 0.01), stroke recurrence (14.3 vs 1.9%, P < 0.001), watershed infarct (15.5 vs 5.4%, P = 0.002), intracranial internal carotid artery (ICA) stenosis (11.9 vs 6.0%, P = 0.041), middle cerebral artery (MCA) stenosis (39.3 vs 22.0%, P < 0.001) and basilar artery (BA) stenosis (16.7 vs 7.1%, P = 0.011). Multivariate analysis indicated that watershed infarcts (OR, 2.85; 95% CI, 1.04-7.81), MCA (OR, 2.23; 95% CI, 1.17-4.25) and BA (OR, 2.86; 95% CI, 1.19-6.87) stenosis or occlusion were independent risk factors for ND, as was pneumonia (OR, 3.4; 95% CI, 1.46-7.9). DISCUSSION: Patients with watershed infarcts and MCA or BA stenosis or occlusion should be monitored closely, and various therapeutic strategies should be administered simultaneously to prevent pneumonia during hospitalisation.

Somatosensory reflex seizures in a patient with hypertrophic cranial pachymeningitis.

Somatosensory-evoked reflex epilepsy is characterized by seizures in response to specific stimuli. It is highly uncommon for somatosensory-evoked focal seizures to be caused by movement or a change in posture. Reflex epilepsy induced by both somatosensory and proprioceptive stimulations has not been previously reported. In this study, we present a case of reflex epilepsy evoked by somatosensory and proprioceptive stimulation in a patient with hypertrophic cranial pachymeningitis. After comparing our patient with other cases of previously reported somatosensory-evoked reflex epilepsy, we determined that our patient had an unusual cause of reflex epilepsy.

Higher numbers of circulating endothelial progenitor cells in stroke patients with intracranial arterial stenosis.

BACKGROUND: Bone marrow-derived endothelial stem cells participate in vascular repairs. Numbers of circulating endothelial progenitor cells (cEPCs) are associated with atherosclerosis. Fibrinogen plays a key role in atherosclerosis. Objective was to assess if cEPC counts were associated with atherosclerotic intracranial artery stenosis (IAS). METHODS: Three hundred subjects (108 patients with stroke and IAS (IAS), 120 control patients with stroke without IAS (CP), and 72 healthy controls (HC)) were retrospectively analyzed. cEPCs were identified and counted by flow cytometry using CD34, CD133 and KDR. Plasma fibrinogen was measured by immunoturbidimetry. cEPC counts were compared between the three groups. RESULTS: cEPC numbers were significantly higher in IAS (0.059 ± 0.031%) than in CP (0.026 ± 0.012%) (P < 0.001) and HC (0.021 ± 0.011%) (P < 0.001), but without difference between CP and HC (P = 0.401). Multiple logistic regression analysis showed that cEPC levels (OR 3.31, 95%CI 1.26-8.87, P = 0.025; IAS vs. CP) were independent markers of IAS after adjustment for hypertension, diabetes and smoking. No significant correlation between cEPC counts and plasma fibrinogen levels was observed (P > 0.05). CONCLUSION: cEPC numbers were associated with degrees of IAS. This measurement may be useful for non-invasive evaluation of atherosclerotic IAS.

Homocysteine and ischemic stroke subtype: a relationship study in Chinese patients.

OBJECTIVE: Elevated homocysteine level is a risk factor for ischemic stroke and associated with small vessel disease such as confluent leukoaraiosis in white and black population. We investigated the relationship between the total serum homocysteine level and ischemic stroke subtypes in Chinese population. METHODS: Three hundred and seventy-seven acute ischemic stroke and 106 transient ischemic attack patients were consecutively enrolled into this study. Demographic information and traditional risk factors were collected. Stroke subtypes were classified using the Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. Leukoaraiosis was graded from 0 to 3 according to the severity. Small vessel disease patients were further categorized into two subgroups of having or without confluent leukoaraiosis. RESULTS: The highest homocysteine level was found in small vessel disease patients after adjusting for age, gender, traditional vascular risk factors and renal function. Homocysteine level was significantly different between the ischemic stroke and transient ischemic attack groups. Elevated homocysteine level was significantly correlated with the severity of leukoaraiosis in all patients with stroke and small vessel disease. Small vessel disease patients with leukoaraiosis had significant higher homocysteine levels than those without leukoaraiosis. CONCLUSIONS: In this group of Chinese patients studied, small vessel disease patients with confluent leukoaraiosis had the highest homocysteine levels.

[Effects of cyclooxygenase-1 inhibitor on spinal ERK expression in rats with postoperative pain].

AIM: To explore the effects of intrathecal injection of selective cyclooxygenase-1 (COX-1) inhibitor, SC-560, on mechanical allo dynia and spinal ERK protein expression in rats with postoperative pain. METHODS: Rats were divided into 4 groups: control group, postoperative pain group, SC-560 group and DMSO group. Mechanical withdrawal threshold (MWT), immunohistochemical and Western blotting technique were used to evaluate mechanical hypersensitivity and the expression of phospho-ERK in the spinal cord, respectively. RESULTS: (1) Behavior test rats developed allodynia 1 h after operation and SC-560 100 microg administrated intrathecally demonstrated a significant reduction in postoperative hypersensitivity. (2) Immunohistochemical staining Phospho-ERK positive neurons in the rat superficial spinal dorsal horn increased significantly 1 h after incision compared with that of non-incision group. Intrathecal administration of SC-560 preoperatively could significantly reduce the number of phospho-ERK positive neurons. (3) Western blot expression of phospho-ERK1/2 protein in the lumbar spinal cord increased significantly 1 h after incision and decreased by intrathecal injection of SC-560. CONCLUSION: SC-560 administrated intrathecally can inhibit mechanical hypersensitivity induced by postoperative pain in rats and this anti-allodynic process may mediated by spinal ERK.