Cerebral venous sinus stenting and jugular bulb embolization for pulsatile tinnitus: A case report.

Background: Pulsatile tinnitus (PT) is a rare form of tinnitus that aligns with the heartbeat. It is typically brought on by lesions with significant vascularity, which produce aberrant sound conduction and increase the risk of mental health issues and hearing loss. Venous PT is more prevalent than arterial PT. Open procedures or interventional procedures can be used to treat PT. We present here a case of PT caused by venous luminal stenosis combined with jugular bulb (JB) malformation, which was improved by stenting and JB embolization. Case presentation: A 59-year-old woman presented with long-term tinnitus consistent with heart rhythm and hearing loss, accompanied by anxiety, insomnia, and depression. The results of brain MRV, CT, and DSA showed stenosis of the right sigmoid sinus and high jugular bulb (JB) with dehiscence of the JB wall. The patient saw a significant improvement in PT symptoms following sigmoid sinus stenting and spring coil embolization of the high JB, following the diagnosis of PT. The patient had no PT recurrence for the course of the 31-month follow-up period. Conclusion: In the present PT case, there was a simultaneous onset of the right sigmoid sinus stenosis and the high JB with the JB wall abnormalities. Sigmoid sinus stenting and spring coil embolization of high JB may be a treatment for the PT, but the prevention of post-stenting complications is still an issue that requires great attention and needs further study.

MTHFR A1298C gene polymorphism on stroke risk: an updated meta-analysis.

BACKGROUND: Previous studies have shown the effect of MTHFR A1298C gene polymorphism on stroke risk. But the results of published studies remained inconclusive and controversial. So we conducted a meta-analysis to accurately estimate the potential association between MTHFR A1298C gene polymorphism and stroke susceptibility. METHODS: A systematic literature search on Embase, Pubmed, Web of Science, Cochrane Library, China National Knowledge Infrastructure (CNKI) and WanFang electronic database identified 40 articles including 5725 cases and 8655 controls. Strength of association was evaluated by pooled odds ratio (OR), 95% confidence interval (CI) and p value. Funnel plots and Begger's regression test were applied for testing the publication bias. Statistical analysis of all data was performed by Stata 12.0. RESULTS: The meta-analysis results indicated a significant relationship between MTHFR gene A1298C polymorphisms and stoke risk under the C allelic genetic model (OR = 1.19, 95%CI = 1.07-1.32, p = 0.001), dominant genetic model (OR = 1.19, 95%CI = 1.06-1.33, p = 0.004) and recessive genetic model (OR = 1.43, 95%CI =1.15-1.77, p = 0.001). In subgroup analysis, we discovered obvious correlation in three genetic model of Asian, stroke type, adult by ethnicity, population, stroke type, source of control and case size. Additionally, in studies of control from hospital and case size equal 100, obvious correlation was also found in the three genetic model. CONCLUSIONS: Our meta-analysis results indicated that there was evidence to support the correlation between MTHFR A1298C polymorphism and stroke susceptibility, especially in adults and ischemic stroke.

New-onset lesions on MRI-DWI and cerebral blood flow changes on 3D-pCASL after carotid artery stenting.

This study aimed to investigate the relationship between the new-onset hyperintense lesions on diffusion-weighted images (DWI) and the changes of cerebral blood flow (CBF) before and after carotid artery stenting (CAS) in patients with symptomatic unilateral carotid artery stenosis. Twenty-four patients with symptomatic unilateral carotid stenosis (50-99%) were enrolled. Routine head magnetic resonance imaging and three-dimensional pseudo-continuous arterial spin labeling were taken 7 days before the surgery and for four consecutive days post CAS. While the incidence of new DWI lesions were high (17/24, 70.8%) and 176 lesions were observed among the 17 cases, there was only one subject showing the symptoms. The majority of the lesions were located at the cortex/subcortex of the ipsilateral frontal and parietal lobes (60.8%) with 92.6% of the lesions size being less than 3 mm. The CBFs in this area were significantly higher than that of the temporal lobe on the first 3 days post stenting (p < 0.05). No periprocedural CBF differences were observed between the two groups, however, the micro-embolism group presented decreased relative CBF in frontal and parietal lobes prior to stenting compared with the non-embolism group. The systolic blood pressure in the micro-embolism group at discharge was significantly lower than that at admission. The high incidence rate of micro-embolism in patients receiving CAS may not be the result of direct changes of hemodynamics in the brain but rather the loss of CBF regulation due to long-term hypoperfusion prior to the stenting.

Altered peri-seizure EEG microstate dynamics in patients with absence epilepsy.

OBJECTIVE: To investigate whether the parameters of EEG microstates changed before and after an absence seizure episode. METHODS: AE patients with a current high frequency of seizures were included (n=21). Each included subject underwent a two-hour and 19-channel video EEG examination. Five epochs of 10-second EEG data in interictal, pre-seizure, and post-seizure states were collected from each AE patient. Five 10-second resting-state EEG epochs from sex- and age-matched HCs who reported no history of neurological or psychiatric disorders and visited the hospital for routine physical examinations were collected. Microstate analysis and source localization of microstates were performed using the LORETA KEY tool. RESULTS: Compared with the resting-state EEGs of HCs, the interictal EEGs of AE patients showed a higher relative transition rate from microstates B to D (p<0.05). From interictal to pre-seizure EEG, the total time ratio of microstate C and the occurrence of microstate B decreased significantly, while the duration of microstate B increased significantly (p<0.05). Compared with pre-seizure EEGs, microstate C in post-seizure EEGs showed a significantly downregulated total time percentage and occurrence (p<0.05). The source localization of each microstate in each condition also varied and showed spatial recovery tends from pre- to post-seizure states. CONCLUSION: Altered EEG microstate dynamics exist between inter-ictal EEGs of AE patients and resting-state EEGs of HCs and between pre- and post-seizure EEGs in AE patients. The EEG microstates of epileptic patients before and after absence seizures are characterized by a "slowdown" in transitions between microstates. Microstates might be used as an index to evaluate the temporal and spatial recovery process of absence seizures in AE.

Physcion Protects Rats Against Cerebral Ischemia-Reperfusion Injury via Inhibition of TLR4/NF-kB Signaling Pathway.

BACKGROUND: Ischemic stroke (IS) is characterized by the rapid loss of brain function due to ischemia. Physcion has been found to have a neuroprotective effect against cerebral ischemia-reperfusion (I/R) injury. However, the mechanism by which physcion regulates cerebral I/R injury remains largely unknown. METHODS: An oxygen-glucose deprivation/reperfusion (OGD/R) model in SH-SY5Y cells and a rat cerebral ischemia-reperfusion (I/R) model were established, respectively. CCK-8 and flow cytometry assays were used to detect the viability and apoptosis of SH-SY5Y cells. Moreover, enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of SOD, MDA, GSH-Px, TNF-α, IL-1ß, IL-6 and IL-10 in the supernatant of SH-SY5Y cells. Meanwhile, Western blot assay was used to detect the expressions of TLR4, p-p65 and p-IκB in SH-SY5Y cells and I/R rats. RESULTS: In this study, physcion treatment significantly rescued OGD/R-induced neuronal injury. In addition, physcion decreased inflammatory response in SH-SY5Y cells after OGD/R insult, as shown by the decreased levels of the pro-inflammatory factors TNF-α, IL-1ß, IL-6 and IL-10. Moreover, physcion attenuated the oxidative stress in OGD/R-treated SY-SY5Y cells, as evidenced by the increased SOD and GSH levels and the decreased ROS and MDA levels. Meanwhile, physcion significantly reduced cerebral infarction, attenuated neuronal injury and apoptosis in I/R rats. Furthermore, physcion markedly decreased the expressions of TLR4, p-NF-κB p65 and p-IκB in the brain tissues of rats subjected to I/R and in SH-SY5Y cells exposed to OGD/R. CONCLUSION: In conclusion, our study indicated that physcion protected neuron cells against I/R injury in vitro and in vivo by inhibition of the TLR4/NF-kB pathway; thus, physcion might serve as a promising therapeutic candidate for IS.

Xiaoyukang Jiaonang Promotes the Degradation of Hypoxia-Inducible Factor 1α and Antiangiogenesis and Anti-Inflammation in Chronic Subdural Hematoma Rat Model.

Xiaoyukang Jiaonang (XYK) is a Chinese patent medicine approved by the National Medical Product Administration which is used to treat intracranial hematoma in China. In this study, we observed the molecular mechanism of XYK in hypoxia-inducible factor 1α (HIF-1α), inflammation and angiogenesis of chronic subdural hematoma (CSDH). The CSDH model was made by using internal iliac vein blood of Wister rats, and rats were divided into sham group, CSDH group and XYK group. The rats in the XYK group were gavaged with Xiaoyukang Jiaonang (185 mg/kg) for 7 days, and rats in the CSDH group and sham group were gavaged with the same amount of physiological saline for 7 days. In the CSHD rat model, active inflammation and angiogenesis were observed around the hematoma. XYK promoted the ubiquitination and degradation of HIF-1α, and reduced the concentration of VEGF and the ratio of angiopoietin-1/angiopoietin-2. XYK reduced proinflammatory cytokines and increased anti-inflammatory cytokine. In tissue section, XYK reduced the size of the hematoma and membrane, and reduced vWF positive cells in membrane. Furthermore, the endothelial progenitor cells in blood decreased as well. Overall, XYK shows anti-inflammatory and antiangiogenesis effects which may relate to the degradation of HIF-1α.

The Pathogenesis of Diabetes Mellitus by Oxidative Stress and Inflammation: Its Inhibition by Berberine.

A substantial knowledge on the pathogenesis of diabetes mellitus (DM) by oxidative stress and inflammation is available. Berberine is a biologically active botanical that can combat oxidative stress and inflammation and thus ameliorate DM, especially type 2 DM. This article describes the potential of berberine against oxidative stress and inflammation with special emphasis on its mechanistic aspects. In diabetic animal studies, the modified levels of proinflammatory cytokines and oxidative stress markers were observed after administering berberine. In renal, fat, hepatic, pancreatic and several others tissues, berberine-mediated suppression of oxidative stress and inflammation was noted. Berberine acted against oxidative stress and inflammation through a very complex mechanism consisting of several kinases and signaling pathways involving various factors, including NF-κB (nuclear factor-κB) and AMPK (AMP-activated protein kinases). Moreover, MAPKs (mitogen-activated protein kinases) and Nrf2 (nuclear factor erythroid-2 related factor 2) also have mechanistic involvement in oxidative stress and inflammation. In spite of above advancements, the mechanistic aspects of the inhibitory role of berberine against oxidative stress and inflammation in diabetes mellitus still necessitate additional molecular studies. These studies will be useful to examine the new prospects of natural moieties against DM.

Application of COMPONT Medical Adhesive Glue for Tension-Reduced Duraplasty in Decompressive Craniotomy.

BACKGROUND The aim of this study was to evaluate the application of medical adhesive glue for tension-reduced duraplasty in decompressive craniotomy. MATERIAL AND METHODS A total of 56 cases were enrolled for this study from Jan 2013 to May 2015. All patients underwent decompressive craniotomy and the dura was repaired in all of them with tension-reduced duraplasty using the COMPONT medical adhesive to glue artificial dura together. The postoperative complications and the healing of dura mater were observed and recorded. RESULTS No wound infection, epidural or subdural hematoma, cerebrospinal fluid leakage, or other complications associated with the procedure occurred, and there were no allergic reactions to the COMPONT medical adhesive glue. The second-phase surgery of cranioplasty was performed at 3 to 6 months after the decompressive craniotomy in 32 out of the 56 cases. During the cranioplasty we observed no adherence of the artificial dura mater patch to the skin flap, no residual COMPONT glue, or hydropic or contracture change of tissue at the surgical sites. Additionally, no defect or weakening of the adherence between the artificial dura mater patch and the self dura matter occurred. CONCLUSIONS COMPONT medical adhesive glue is a safe and reliable tool for tension-reduced duraplasty in decompressive craniotomy.

[Clinical-diffusion mismatch and short-term clinical outcomes among patients with acute ischemic stroke].

OBJECTIVE: To explore the law of clinical-diffusion mismatch (CDM) among patients with acute ischemic stroke (AIS) and analyze the relationships between CDM and short-term clinical outcomes. METHODS: A prospective study was conducted for 56 patients with AIS admitted into our hospital within 72 hours from March 2011 to March 2012. And brain magnetic resonance imaging (MRI) examinations were completed within one week. All cases were diagnosed with infarction in the area of middle cerebral artery (MCA). The diffusion-weighted imaging (DWI) volume was calculated by semi-automatic method. Also the scores of National Institutes of Health stroke Scale (NIHSS) and modified Rankin Scale (mRS) were scored at baseline, days 7, 15, 30 post-admission respectively. The non-parametric variables were analyzed by Spearman's rank correlation. And the differences for non-parametric variables between CDM and non-CDM groups were analyzed by Mann-Whitney rank-sum test. RESULTS: A total of 16/56(28.6%) patients showed CDM. The CDM ratios of the patients undergoing MRI within 72 hours after onset and those beyond 72 hours after onset were 36.3% and 17.4% respectively. Also 50.0% of those with CDM had favorite neurological outcomes. While for the other group without CDM, only 6.7% did so. The differences were significant (P = 0.001). The correlations for all AIS patients between NIHSS scores and DWI volume were strong (rs = 0.721, P = 0.009). Specifically, the correlations for without CDM group (rs = 0.847, P = 0.000) were stronger than those of with CDM group (rs = 0.610, P = 0.012). No significant inter-group differences existed in favorite clinical outcome, mortality case or neurological deterioration. CONCLUSION: CDM still occurs within 1 week after onset among patients with AIS. Although no significant differences exist in favorite clinical outcome between patients with CDM and without CDM, the CDM group may improve more in NIHSS scores and have better neurological outcomes.

[Expression and effect of neuropilin-1 in acute myeloid leukemic cells].

This study was aimed to investigate the expression of neuropilin-1 (NRP-1) and NRP-2 mRNA in myeloid leukemia cells and the effect of NRP-1 on cell proliferation and migration. The expressions of NRP-1 and NRP-2 mRNA in bone marrow mononuclear cells of 24 patients with acute myeloid leukemia and in 7 myeloid leukemic cell lines (HL-60, KGIa, NB4, U937, HEL MEG01 and K562) were detected by RT-PCR. The effects of NRP-1 interfered with siRNA on proliferation and migration in leukemic cell line HEL were examined by MTT and migration test. The results showed that the expression of NRP-1 mRNA was found in bone marrow mononuclear cells (BMMNCS) of 24 AML patients, the positive rate was 100% and significantly higher than that in control group (positive rate 67%). The expressions of NRP-2 mRNA were seen in 79% AML patients and in 67% health control, there was no significant difference between them. The increased NRP-1 expression was directly correlated with the blast percentage in both peripheral blood and bone marrow of AML patients (r=05, r=0.4, p<0.05). The expressions of NRP-1 and NRP-2 mRNA were observed in 6/7 and 3/7 myeloid leukemic cell lines respectively. After HEL cells were transfected with siRNA for 24 hours, the expression levels of NRP-1 mRNA and protein decreased obviously. Under VEGF action, the cell number in control group significantly increased, while the cell proliferation in interfered group had been not changed. After being transfected for 24 hours, the migration in interfered group decreased significantly. It is concluded that the higher level of NRP-1 mRNA is expressed in bone marrow mononuclear cells of leukemia patients and plays a pivotal role in proliferation and migration of myeloid leukemic cells. Inhibition of NRP-1 functions may provide a new therapeutic strategy for AML.

Human umbilical cord blood cells express neurotrophic factors.

Freshly isolated or culture-expanded human umbilical cord blood mononuclear cells (CBMNCs) have been known to express neural phenotypes in vitro and to differentiate into neural cells and improve neurological function recovery after being administrated into rodent models of neurological diseases. However, the mechanism of action remains unclear. The present study observed that CBMNCs expressed higher level mRNAs of several neurotrophic factors than adult peripheral blood mononuclear cells (PBMCs). In addition, a significantly increase in the levels of brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT4/5) was found in culture supernatants of CBMNCs compared to that of PBMNCs. These findings indicate that CBMNCs express several neurotrophic factors and suggest that the neurotrophic factors secreted by CBMNCs may be responsible for amelioration of central nervous system deficits in animal models after CBMNC administration.