Dehydration in cerebral venous sinus thrombosis.

AIMS: This study aimed to unravel the dehydration status of patients with cerebral venous sinus thrombosis (CVST) to facilitate the understanding of dehydration in CVST. METHODS: This was a multicenter retrospective study and three populations were recruited, namely, patients with CVST, CVST mimics, and healthy subjects. Blood samples were obtained 1-2 days after admission to assess dehydration status. Stata 15.1 was performed for statistical analysis. RESULTS: A total of 208 patients were diagnosed with CVST, 237 with CVST mimics, and 200 healthy individuals were enrolled. The urine specific gravity (USG, 1.020 [1.014, 1.029] vs. 1.017 [1.011, 1.021]) was higher in patients with CVST than in those with mimics (all p < 0.001). The percentage of USG >1.03 was also higher in CVST (22.6%) than in its mimics (6.3%, p < 0.001). With the development of CVST, USG (acute vs. sub-acute vs. chronic, 1.022 [1.015, 1.033] vs. 1.021 [1.015, 1.031] vs. 1.019 [1.014, 1.025]) decreased. All dehydration-related markers could not differentiate CVST from its mimics and healthy populations, and they were not associated with CVST severity and prognosis (p > 0.05). CONCLUSION: High levels of USG, especially USG >1.013, were more common in patients with CVST. Dehydration-related indices could not characterize CVST and were not associated with CVST severity and prognosis.

Neuroinflammation and anti-inflammatory therapy for ischemic stroke.

Stroke remains one of the most devastating and challenging neurological diseases worldwide. Inflammation, as well as oxidative stress is one of the main contributors to post-stroke injuries, and oxidative stress can further induce inflammation. Moreover, the inflammatory response is closely related to immune modulation in ischemic stroke progression. Hence, major ischemic stroke treatment strategies include targeting inflammatory responses, immune modulation (especially immune cells), and inflammatory response to suppress stroke progression. To date, several drugs have demonstrated clinical efficacy, such as Etanercept and Fingolimod. However, only edaravone dexborneol has successfully passed the phase III clinical trial and been approved by the National Medical Products Administration (NMPA) to treat ischemic stroke in China, which can restore redox balance and regulate inflammatory immune responses, thus providing neuroprotection in ischemic stroke. In this review, we will comprehensively summarize the current advances in the application of inflammatory biomarkers, neuroinflammation and neuro-immunotherapeutic scenarios for ischemic stroke, thus aiming to provide a theoretical basis and new prospects and frontiers for clinical applications.

Association between inflammatory biomarkers and venous thromboembolism: a systematic review and meta-analysis.

BACKGROUND: Venous thromboembolism (VTE) is a common thrombotic vascular disease that has a significant impact on people's well-being and quality of life. A plethora of clinical studies explore the relationship between inflammatory biomarkers and VTE but yield conflicting results. This article proposed to pool these studies to draw a more convincing conclusion. METHODS: We searched several databases for studies before April 2023. Available data was processed using Stata software (version 15.0 SE) and R (version 4.1.2). This meta-analysis has been registered in PROSPERO (CRD42022321815). The VTE in this review encompassed pulmonary embolism, deep vein thrombosis, and cerebral venous thrombosis. RESULTS: A total of 25 articles were finally involved in this study. Our results revealed that higher levels of high-sensitivity C-reactive protein (hs-CRP, MD, 0.63, 95%CI, 0.21-1.05) and C-reactive protein (CRP)> 3ug/ml (OR, 1.52, 95%CI, 1.18-1.96) might be regarded as risk factors for future VTE occurrence. The elevated levels of monocyte (MD, 0.03, 95%CI, 0.00-0.05), hs-CRP (0.85, 0.61-1.08), CRP (0.66, 0.20-1.13) and IL-6 (0.47, 0.25-0.70) might represent the previous VTE; a series of markers such as white blood cell (1.43, 0.88-1.98), neutrophil (1.79, 1.02-2.56), monocyte (0.17, 0.14-0.21), hs-CRP (3.72, 1.45-5.99), IL-6 (5.99, 4.52-7.46), platelet-lymphocyte ratio (33.1, 24.45-41.78) and neutrophil-lymphocyte ratio (1.34, 0.95-1.73) increased during the acute phase of VTE. CONCLUSIONS: In general, activated inflammatory biomarkers might not only be correlated with an increased risk of VTE, but may also give a hint of the occurrence of VTE in clinical settings.

LncRNA Expression Profiling of Ischemic Stroke During the Transition From the Acute to Subacute Stage.

Ischemic stroke induces profound effects on the peripheral immune system, which may participate the infectious complications. However, the exact function and mechanism of immune reaction in stroke development are not well-elucidated. Recently, several long non-coding RNAs (LncRNAs) are reported to affect ischemic stroke process, especially the immunological response after stroke. In the present study, we investigated the profile of LncRNAs in human ischemic stroke during the transition from the acute to subacute stage, when the state of the peripheral immune system changes from activation to systemic immunosuppression. In this study, we analyzed the RNA-sequencing (RNA-seq) datasets obtained at two time points (24 h and 7 days) from the peripheral blood mononuclear cells of ischemic patients. Vascular risk factor-matched healthy adults were enrolled as controls. A total of 3,009 LncRNAs and 3,982 mRNAs were identified as differentially expressed 24 h after stroke. Furthermore, 2,034 LncRNAs and 1,641 mRNAs were detected to be differentially expressed on day 7. Bioinformatics analyses, including GO, KEGG pathway enrichment analysis, and network analysis, were performed for the identified dysregulated genes. Our study reveals that ischemic stroke can influence the expression of LncRNAs and mRNAs in the peripheral blood at both the acute and subacute stages; the level of LncRNAs in the antigen processing and presentation pathway was clearly upregulated at 24 h and had recovered to normal levels on day 7 after stroke. Moreover, inflammatory mediator regulation of TRP channels and GABAergic synapses were two specifically downregulated pathways on day 7 after stroke. Our findings provide a valuable resource for further study of the role of LncRNAs in peripheral immune system changes following ischemic stroke.

Multiple intracranial arterial stenosis influences the long-term prognosis of symptomatic middle cerebral artery occlusion.

BACKGROUND: Large intracranial occlusive vascular disease is a major contributor to the incidence of stroke worldwide, especially when it involves the middle cerebral artery (MCA). The data on the prognosis of symptomatic atherosclerotic MCA occlusions (MCAO) with concomitant intracranial arterial disease (MCAO-AIS) are limited. MCAO-AIS may reflect the extent of the atherosclerotic intracranial disease, we hypotheses that coexisting intracranial arterial disease influenced the prognosis of MCAO. METHODS: Patients having survived at least one month after the initial ischemic stroke who suffered from atherosclerotic occlusion of the MCA were enrolled. According to their concomitant atherosclerotic intracranial arterial disease, the patients were assigned to one of two groups: the MCAO or the MCAO-AIS. All of the patients' cerebrovascular risk factors were recorded. Recurrent ischemic stroke and death were the end-point events during the follow-up. RESULTS: A total of 232 patients (mean age 57.68 ± 9.50 years; 69% male) were analyzed. The mean follow-up time was 17.65 months. The end-point events occurred in 35 (15.09%) patients, resulting in an annual rate of 10.26%. The presence of MCAO- AIS was an independent risk factor associated with the patient's prognosis in the cohort (OR = 3.426, 95% CI 1.261 to 9.308; p = 0.016), as well as gender and diabetes mellitus. The MCAO-AIS were more likely to experience ipsilateral ischemic strokes, but the difference was not statistically significant. CONCLUSION: Concomitant intracranial arterial disease may influence the prognosis of patients with atherosclerotic MCAO. The result warrants further research in larger sample population.

Chromosome 9p21.3 Variants Are Associated with Cerebral Infarction in Chinese Population.

Common variants of chromosome 9p21.3 associated with coronary disease have been established, but the association of 9p21.3 and cerebral infarction (CI) is not consistent. The aim of this study is to confirm the association of cerebral infarction and 9p21.3 in a Chinese Han population. This is a hospital-based case-control study, which involves 769 patients and 682 healthy controls. Eight single-nucleotide polymorphisms (SNPs) associated with cerebral infarction in previous literatures were genotyped and analyzed. The association analyses were performed at both SNP and haplotype levels. Three (rs2383207, rs1537378, and rs3731245) of eight SNPs were associated with cerebral infarction. In an allelic association analysis, rs2383207, rs3731245, and rs1537378 were significantly associated with CI; the odd ratios were 1.18 (95 % confidence interval (CI) = 1.01-1.37, P = 0.04), 1.29 (95 % CI = 1.06-1.56, P = 0.01), and 1.30 (95 % CI = 1.05-1.60, P = 0.02), respectively. rs1537378 remains significantly associated with CI independent of traditional cerebrovascular risk factors in a recessive model (odds ratio (OR) = 1.35, 95 % CI = 1.06-1.71, P = 0.013, Q = 0.03) and in an additive model (OR = 1.38, 95 % CI = 1.11-1.71, P = 0.004, Q = 0.02); conversely, rs2383207 (OR = 1.28, 95 % CI = 1.03-1.59, P = 0.02, Q = 0.03) and rs3731245 (OR = 1.31, 95 % CI = 1.05-1.65, P = 0.02, Q = 0.03) were significantly different in a recessive model. Haplotype analysis showed that the protective effect for haplotype AATAA remained significant (OR = 0.87, 95 % CI = 0.73-1.00, P = 2.99 × 10(3), Q = 2.15 × 10(3)). These findings showed that chromosome 9p21.3 is an important susceptibility locus for cerebral infarction in Chinese population.

Ranitidine reduced levodopa-induced dyskinesia in a rat model of Parkinson's disease.

BACKGROUND: Chronic administration of levodopa in Parkinson's disease leads to debilitating involuntary movements, termed levodopa-induced dyskinesia (LID). The pathogenesis of LID is poorly understood. Previous research has shown that histamine H2 receptors are highly expressed in the input (striatum) and output (globus pallidus, substantia nigra) regions of the basal ganglia, particularly in the GABAergic striatopallidal and striatonigral pathways. Therefore, a histamine H2 receptor antagonist could be used to reduce LID. In the present work, we investigated whether ranitidine has the potential to diminish LID in rats with dyskinesia and explored the underlying mechanisms involved. METHODS: A rat model of PD was induced by 6-hydroxydopamine. Valid PD rats were then treated with levodopa (25 mg/kg, intraperitoneally) and benserazide (12.5 mg/kg, intraperitoneally) for 21 days to induce a rat model of LID. The acute and chronic effects of administration of ranitidine at different doses (5 mg/kg, 10 mg/kg, and 20 mg/kg) on abnormal involuntary movements, levodopa-induced rotations, and the forelimb adjusting steps test were investigated in LID rats. The chronic effect of ranitidine (10 mg/kg) on the expression of Arc and proenkephalin was also evaluated. RESULTS: Levodopa elicited increased dyskinesia in PD rats. Acute ranitidine treatment had no effect on LID, but chronic ranitidine administration (10 mg/kg, 20 mg/kg) reduced LID in rats with dyskinesia. Importantly, levodopa-induced rotations were not affected by chronic treatment with ranitidine. In addition, chronic ranitidine (10 mg/kg, 20 mg/kg) significantly improved stepping of the lesioned forepaw. Real-time polymerase chain reaction showed that Arc and proenkephalin levels were reduced by chronic ranitidine (10 mg/kg) in dyskinetic rats. CONCLUSION: These data indicate that ranitidine is a good adjunct for reducing LID in rats with dyskinesia. Inhibition of dopamine D1-mediated activation in the medium spiny neurons may account for the antidyskinetic effects of ranitidine in rats with dyskinesia.

Intranasal administration of nerve growth factor ameliorate ß-amyloid deposition after traumatic brain injury in rats.

The marked increase of amyloid-ß (Aß) peptide after traumatic brain injury (TBI), confers a risk factor for Alzheimer's disease (AD) in patients' later life. Nerve growth factor (NGF) is great potential to repair brain injury. But its clinical application is limited because of lacking feasible methods for delivering NGF into brain. This study investigated the effects of NGF, delivered intranasally, on the Aß burden in the injured ipsilateral cortex and hippocampus of rats with TBI. Adult male Sprague-Dawley rats were subjected to the modified Feeney's weight-drop model and treated without or with NGF by intranasal route. Motor and cognitive functional outcome, immunostaining, ELISA assay and western blot were performed. Compared to sham operated rats, TBI rats exhibited significantly increased APP and Aß42 expression as well as decreased functional outcome after TBI. Intranasal administration of NGF significantly attenuated Aß42 deposits, and improved functional outcome after TBI. Thus, intranasal delivery of NGF provides a potential strategy for reducing the risk of developing AD in the later life of TBI patients.

Association between plasma homocysteine levels and obstructive sleep apnoea in patients with ischaemic stroke.

We aimed to investigate the association between plasma homocysteine and obstructive sleep apnoea (OSA) syndrome in patients with ischaemic stroke. A total of 102 patients with ischaemic stroke were classified into four OSA groups based on their apnoea-hypopnoea index (AHI): absent (AHI < 5/hour); mild (5-14/hour); moderate (15-30/hour); and severe (> 30/hour). The mean (± standard deviation) homocysteine levels in the four OSA groups were: absent, 8.98 ± 3.74 µmol/L; mild, 11.46 ± 3.31 µmol/L; moderate, 14.18 ± 4.36 µmol/L; and severe, 18.57 ± 4.56 µmol/L; and these differences were statistically significant (p < 0.001). The Pearson correlation analysis revealed a positive correlation between homocysteine levels and the severity of AHI (r = 0.482, p < 0.001). Multiple linear regression analysis showed that AHI and folate were independent predictors of homocysteine levels (R(2) = 0.539, p < 0.001, ß for AHI = 0.259, ß for folate = -0.400). In conclusion, the severity of OSA is significantly associated with elevated homocysteine levels in patients with ischaemic stroke, and this association is independent of other factors that cause elevation in homocysteine.

Intranasal ginsenoside Rb1 targets the brain and ameliorates cerebral ischemia/reperfusion injury in rats.

Ginsenoside Rb1 (GRb1) has been shown to benefit many central nervous system (CNS) disorders, including stroke. However, its bioavailability is low after oral administration due to poor absorption. Intranasal administration has been considered as an effective method for central nervous system drug delivery for its brain-targeting effect. Here, whether intranasal GRb1 could ameliorate cerebral ischemia/reperfusion injury was investigated. First, the concentration of GRb1 in brain tissues and plasma after intranasal and intravenous delivery was calculated using HPLC-MS/MS methods in male Sprague-Dawley rats (250±10 g). Intranasal GRb1 was considered brain-targeting if the value of the drug targeting index (DTI) was greater than 1. Rats were subjected to 1.5 h middle cerebral artery occlusion (MCAO) and were killed 24 h after reperfusion. The neuroprotective effects were measured using 2,3,5-triphenyltetrazolium chloride (TTC) staining and Nissl staining. Immunoblotting of LC3 and Beclin 1, crucial autophagy-related proteins, was used to monitor the state of autophagy. With a local bioavailability of 10.28-32.48% and DTI of 7.35-23.22 in different brain regions, intranasal GRb1 was determined to be brain-targeting. Less infarct volume and more intact neuronal structure were observed in the GRb1 group. GRb1 also restored the elevation of LC3 and Beclin 1. Our work suggests that intranasal GRb1 exerts brain-targeting effects and that a single dose of intranasal GRb1 immediately after MCAO ameliorates ischemia/reperfusion insult. Autophagy is involved in these beneficial effects.

Evaluation of angiographic changes of the anterior choroidal and posterior communicating arteries for predicting cerebrovascular lesions in adult moyamoya disease.

To ascertain the relationship between angiographic changes of the anterior choroidal and posterior communicating arteries (AChA-PComA) and cerebrovascular lesions in adult patients with moyamoya disease (MMD), we reviewed cerebral angiograms from 132 adult patients with MMD (68 with ischemia and 64 with hemorrhage). The angiographic findings of the AChA-PComA in each symptomatic hemisphere were graded on a scale of 0 to 3. The data were statistically analyzed for correlation with cerebrovascular lesions. Extension with abnormal branches and excessive dilation of the AChA-PComA accounted for 28 of the hemorrhagic lesions (28/64, 43.8%), especially intraventricular hemorrhage (16/28, 57.1%; p<0.001). Additionally, when the occlusion was proximal to the PComA of the internal carotid artery, the posterior circulation territory was susceptible to ischemic lesions or subarachnoid hemorrhage (SAH) (p<0.001), particularly aneurysmal SAH (p<0.001). The angiographic characteristics of AChA-PComA may predict the onset of certain cerebrovascular lesions in adult patients with MMD.

Angioplasty and stenting for the occluded internal carotid artery.

To investigate the feasibility and efficacy of angioplasty and stenting for symptomatic occlusion of carotid artery. From December 2004 to June 2009, 17 patients with progressive or reoccurred ischemic stroke or repeated transient ischemic attack resulted from the total occluded carotid artery underwent angioplasty and stenting were reviewed. All patients with successful procedure were followed up. Clinic and angiography data were documented prospectively. The median time from symptoms onset to procedure was 23 days (range 3-94 days). Twelve of the 17 patients (70%) were obtained technique success. Eight patients were observed the collapse of internal carotid artery between occluded location to origin of ophthalmic artery after the occlusion was patent. Two patients had clots which were solved with urokinase. The collapsed internal carotid artery was improved markedly in the compute tomography angiograph 7 days after the procedure. No any complications related procedures occurred. One patient died from myocardial infarct and one suffered from ischemic minor stroke in brainstem for a median follow-up of 346.5 days. One of 9 patients (11.1%) was observed in-stent stenosis in the follow-up angiography. Angioplasty and stenting was a potential alternative therapy for symptomatic occlusion of carotid artery. Further study is required to determine the safety of this treatment.

Comparison of BMSs with SES for symptomatic intracranial disease of the middle cerebral artery stenosis.

This study was designed to compare the clinical and angiographic outcomes of patients with symptomatic atherosclerotic middle cerebral artery stenosis treated with balloon-mounted stents (BMS) and self-expandable Wingspan system (SES). We reviewed the 69 consecutive stent placement procedures for symptomatic atherosclerotic stenosis (≥70) in M1 segment of middle cerebral artery in 67 patients in 3 years. According to the stent types, the patients were classed as BMS and SES groups. The demographic characteristics, conventional risk factors of ischemic stroke, degree of stenosis, periprocedural complications, stent types, and clinical and angiographic outcomes were analyzed. There were 39 patients in the BMS group and 28 patients in the SES group. The demographic characteristics, conventional risk factors, and periprocedural complications were similar but different in residual stenosis after stenting in both groups (5.9% ± 9.9% vs. 14.4% ± 14.6%; P = 0.01). For the overall cohort, the rate of stroke or death and restenosis was 10.9% (7/66) and 24.5% (14/57), respectively. The frequency of restenosis was higher in the SES group than in the BMS group (log-rank, P = 0.04; crude hazard ratio = 3.03; 95% confidence interval (CI), 1.01-9.15; P = 0.049; and adjusted hazard ratio = 3.61; 95% CI, 1.06-12.27; P = 0.04); however, there was no difference in clinical outcomes (log-rank, P = 0.51; crude hazard ratio = 1.66; 95% CI, 0.36-7.61; P = 0.51; and adjusted hazard ratio = 0.59; 95% CI, 0.04-7.89; P = 0.69). The corrected degree of restenosis was higher in the SES than the BMS group. The prevalence of restenosis was higher in the SES than the BMS group, but the perioperative complications and follow-up clinical outcomes had no significant difference.

Influence of residual stenosis on clinical outcome and restenosis after middle cerebral artery stenting.

BACKGROUND: The purpose of this study was to assess whether the residual stenosis has effect on restenosis after stenting for atherosclerotic stenosis in the middle cerebral artery. METHODS: Sixty-seven patients underwent 69 single-stent procedures successfully for atherosclerotic stenosis ≥70% in the M1 segment of middle cerebral artery were reviewed retrospectively. All patients were classified into two groups: nonresidual (≤30%) and residual (>30%) stenosis. The influence of residual stenosis immediately after stent placement on clinical outcomes and restenosis at follow-up was analyzed. Restenosis was defined as ≥20% stenosis on angiographic follow-up imaging after excluding postoperative residual stenosis. RESULTS: Between groups, it was no difference in the conventional risk factors of cerebrovascular diseases, characteristics of targeted vessels, and types of stent. The residual stenosis had no influence on any stroke or death, but the ipsilateral stroke had a trend in the residual stenosis group. The incidence of restenosis was higher in patients with residual stenosis >30% (17% vs. 45.5%, P = 0.04), and the increase of percent stenosis was 7.9 ± 11.7 and 17.1 ± 15.4, respectively (P = 0.03). The correlation coefficient was r = 0.37 (P < 0.01) between the residual stenosis and the increase of percent stenosis. Univariate and multivariate regression analysis showed that residual stenosis >30% was an independent risk factor for restenosis at follow-up (log-rank, Chi-square = 6.09, P = 0.01). CONCLUSIONS: Residual stenosis immediately after stenting for atherosclerotic middle cerebral artery stenosis may be a predictor of clinical outcomes and restenosis at follow-up.

Decreased serum brain-derived neurotrophic factor (BDNF) is associated with post-stroke depression but not with BDNF gene Val66Met polymorphism.

BACKGROUND: Decreased brain-derived neurotrophic factor (BDNF) has been demonstrated in animal models and patients with depression. However, little is known about changes in BDNF in post-stroke depression (PSD). This study investigated the changes in serum BDNF in patients with PSD, and evaluated whether serum concentrations of BDNF were associated with BDNF gene Val66Met polymorphism. METHODS: PSD patients were diagnosed in accordance with DSM-IV criteria, and the severity of depression was evaluated with the Hamilton Rating Scale for depression. Serum BDNF was measured twice, first at 7 days after the onset of stroke and then at 3-6 months after stroke. Val66Met polymorphisms of the BDNF gene were determined using the polymerase chain reaction-restriction fragment length polymorphism method. BDNF concentrations and Val66Met polymorphisms were also measured in 30 healthly controls. RESULTS: A total of 93 patients admitted as a result of first time acute ischemic stroke were included. During the 6-month follow-up, 35 patients (37.6%) were diagnosed with PSD. Serum BDNF concentrations were decreased in PSD patients at 3-6 months after stroke (p < 0.05). The serum BDNF concentrations were not associated with BDNF gene Val66Met polymorphisms in either patients or healthy controls. CONCLUSIONS: Serum concentrations of BDNF decrease in PSD patients and BDNF may play an important role in the pathogenesis of PSD. However, Val66Met polymorphisms are not associated with serum concentrations of BDNF. The mechanism of decreased serum BDNF requires further study.

Hyperintense vessels on FLAIR: a useful non-invasive method for assessing intracerebral collaterals.

OBJECTIVE: This study was aimed to evaluate relationship between hyperintense vessels (HV) on fluid-attenuated inversion recovery (FLAIR) and artery steno-occlusion related intracerebral collaterals. MATERIALS AND METHODS: A total of 233 patients with 260 atherosclerotic lesions in the M1 segment of the middle cerebral artery (MCA) were examined with FLAIR and digital subtraction angiography (DSA). HV were graded as 0, 1, 2 and 3 by its distributions in the MCA territory. Grade 0 indicated no HV; Grade 1 indicated the HV limited in Sylvian fissure; Grade 2 indicated the HV limited in Sylvian fissure and the temporal-occipital junction; Grade 3 indicated the HV extended to frontal-parietal lobes. Collateral blood flows were classified by DSA results. The relationship between HV grades and patterns of collateral flows was analyzed. RESULTS: HV were observed in 76 out of 260 hemispheres. For patients with Grade 1 HV, most of their collateral flows (80.8%) were antegrade; for patients with Grade 2, the retrograde leptomeningeal flows were commonly manifested as anterior cerebral artery to MCA (75%); for patients with Grade 3 HV, most of the retrograde leptomeningeal flows were manifested as posterior cerebral artery to MCA (81.8%). As the grade HV increased, the frequency of retrograde leptomeningeal collateral from ACA to MCA decreased (100% to 75% and to 18.2%), and increased (0% to 25% and to 81.8%) for the retrograde leptomeningeal collateral via PCA to MCA (P<0.001). CONCLUSIONS: The HV could assess non-invasively intracerebral collaterals in patients with steno-occlusive lesions of M1 segment of MCA.

Influence of vessel size and tortuosity on in-stent restenosis after stent implantation in the vertebral artery ostium.

PURPOSE: Percutaneous transluminal angioplasty and stenting is emerging as an alternative for treating atherosclerotic stenosis in the vertebral artery ostium. However, in-stent restenosis (ISR) still remains a critical issue to be addressed. Little is known about the relationship between anatomic characteristics of the artery and ISR after stent implantation. In this study, we have evaluated influential factors for ISR in a cohort of the patients with stenting in the vertebral artery ostium. METHODS: Sixty-one patients with 63 symptomatic lesions in vertebral artery ostium treated with stenting were enrolled onto this study. An average of 12.5 months' clinical and angiographic follow-up results were analyzed retrospectively. The possible influential factors for ISR, including conventional risk factors of cerebrovascular diseases and morphological characteristics of target lesions, were evaluated by univariate and multivariate regression analysis. RESULTS: Technical success was achieved in all 63 interventional procedures. Stenosis was reduced from (mean±standard deviation) 75.5±12% before to 1±3.6% after the procedure. During the mean 12.5-month angiographic follow-up, ISR was detected in 17 treated vessels (27.0%), with 2 treated arteries (3.2%) resulting in occlusion, and a stent fracture in 1 case (1.6%). Multivariate Cox regression analysis showed that the tortuosity of V1 (hazard ratio 3.54, P=0.01) and smaller diameter of the stent (hazard ratio 3.8, P=0.04) were independent predictors of ISR. CONCLUSIONS: Angioplasty and stenting for symptomatic stenosis in the vertebral artery ostium stenosis seem to be feasible and effective. Tortuosity and smaller diameter may affect ISR after stent implantation.

Neuroprotective effect of ginsenoside Rb1 on glutamate-induced neurotoxicity: with emphasis on autophagy.

Ginsenoside Rb1 has been demonstrated with neuroprotective effects, but the mechanisms remain unclear. This study aimed to probe the effects and mechanisms of ginsenoside Rb1 on activation of autophagy in glutamate-injured neurons. Ginsenoside Rb1 of exponential concentrations (1.2, 12, 120 microM) or autophagy inhibitor 3-methyladenine (5mM) was added to culture medium for cortical neurons after being treated with glutamate. Cell viability was measured by MTT assay. Autophagosomes formation was observed with transmission electron microscope. Autophagy marked protein LC3 was detected with immunofluorescence and visualized under laser confocal microscopy. Changes of autophagy related protein Beclin-1 were measured with Western blot. We found that ginsenoside Rb1 protected cortical neurons from glutamate-induced cell injury. Autophagy was activated after glutamate treatment, with both autophagosomes and punctate LC3 increased significantly compared with control. Beclin-1 was elevated in glutamate-treated cells. Formation of autophagosome and punctate LC3 was attenuated by ginsenoside Rb1. The level of Beclin-1 in ginsenoside Rb1 treated cells was simultaneously decreased compared with glutamate-treated cells. These results suggested that inhibition of autophagy could be responsible for neuroprotective effects of ginsenoside Rb1 in glutamate-induced injury. Down-regulation of Beclin-1 may play an important role in this process.

[Influencing factors for cerebral microbleeds in patients with acute ischemic stroke].

OBJECTIVE: To investigate the relationship between cerebral microbleeds (CMB), cardiovascular risk factors, and plasma fibrinogen in patients with acute ischemic stroke. METHODS: Sixty-eight patients with acute ischemic stroke from June 2008 to March 2009 were enroued prospectively. All patients received cranial magnetic resonance imaging at the first week, and T2(*)-weighted gradient echo MRI sequence was performed to detect CMB. Plasma fibrinogen, uric acid levels and other biochemical parameters were measured on the next day of admission. All data were selected from Nanjing Stroke Registry Program. RESULTS: Among a total 68 patients, 29 (43%) patients had 109 lesions of cerebral microbleeds on gradient-echo MRI. Age, hypertension, fibrinogen and uric acid were significantly associated with the presence of CMB (P = 0.004, 0.024, 0.020, 0.027 respectively). Through a logistic regression analysis, age, hypertension and plasma fibrinogen were significantly associated with the presence of cerebral microbleeds [(P = 0.02, OR = 1.10, 95%CI 1.02 to 1.19; P = 0.003, OR = 9.35, 95%CI 2.17 to 40.23; P = 0.019, OR = 1.01, 95%CI 1.00 to 1.02]. CONCLUSION: There is a high prevalence of CMB in patients with acute ischemic stroke. And it has a strong relationship with high plasma fibrinogen.