ABSTRACT
Objective:To investigate the predictors of intracranial hemorrhage in patients with cerebral venous sinus thrombosis (CVST).Methods:Patients with CVST treated in Drum Tower Hospital Affiliated to Medical School of Nanjing University from January 2008 to March 2021 were retrospectively enrolled. The risk factors, clinical manifestations, imaging examination and 90 d follow-up data were collected. The complicated intracranial hemorrhage group and non-intracranial hemorrhage group were compared. Multivariate logistic regression analysis was used to determine the independent predictors of intracranial hemorrhage in patients with CVST. Results:A total of 104 patients with CVST were enrolled, including 42 males and 62 females. Their age was 35.24 ± 10.92 years old (range 22-68 years). Thirty-eight patients (36.84%) were complicated with intracranial hemorrhage, including 34 hemorrhagic cerebral infarction and 4 complicated subarachnoid hemorrhage. Univariate analysis showed that compared with the non-intracerebral hemorrhage group, the intracranial hemorrhage group was more common in puerperal/pregnant patients (60.52% vs. 48.48%; P=0.012), with more acute onset (57.89% vs. 48.48%; P=0.004), focal neurological signs (47.37% vs. 19.70%; P=0.003) and seizure (39.47% vs. 18.18%; P=0.017), and the site of thrombosis was more common in the superior sagittal sinus (57.89% vs. 36.36%; P=0.033). Multivariate logistic regression analysis showed that puerperium/pregnancy (odds ratio 2.857, 95% confidence interval 1.095-7.453; P=0.031) and superior sagittal sinus thrombosis (odds ratio 2.847, 95% confidence interval 1.110-7.302; P=0.027) were the independent predictors of intracranial hemorrhage in patients with CVST. The analysis at 90 d after onset showed that there was no significant difference in the good outcome rate between the intracranial hemorrhage group and the non-intracranial hemorrhage group (86.84% vs. 89.39%; P=0.695). Conclusions:Puerperium/pregnancy and superior sagittalsinus thrombosis are the independent risk factors for intracranial hemorrhage in patients with CVST. However, complicated with intracranial hemorrhage is not associated with 90-day clinical outcomes.
ABSTRACT
Objective:To investigate the effect of cocaine- and amphetamine-regulated transcript peptide (CART) on the synapse structure of mice cortical neuron subjected to oxygen-glucose deprivation (OGD).Methods:Primary neurons of the embryonic cerebral cortex obtained from healthy and clean Kunming mice at gestational age of 16-17 d were cultured. They were divided into control group, CART group, OGD group, and OGD+ CART group. 0.4 nmol/L CART 55-102 was added and cultured for 12 h after OGD treatment in the OGD+ CART group; the CART group was given the same dose of CART 55-102. The neuronal mortality was measured by the flow cytometry. The changes of synaptic structure were observed by immunofluorescence analysis, and the axon length and synapsin Ⅰ positive area were quantitatively analyzed. Real-time fluorescent quantitative polymerase chain reaction and Western blot analysis were used to identify the brain-derived neurotrophic factor (BDNF) mRNA and protein expression. Results:Compared with the control group, the mortality of neurons in the OGD group was significantly increased, the neuronal synapse growth was significantly inhibited, the positive area of synapsin Ⅰ was significantly reduced, and the expression levels of BDNF mRNA and protein were significantly down-regulated (all P<0.05). Compared with the OGD group, adding CART 55-102 significantly reduced the mortality of OGD neurons ( P<0.05), reversed the inhibitory effect of OGD on neuronal synapse growth, significantly increased the length of neuron axons and the positive area of synapsin Ⅰ (all P<0.05), and significantly up-regulated BDNF mRNA and protein expression levels (all P<0.05). Conclusion:CART can protect the synaptic structure of mice cortical neuron subjected to OGD, and its mechanism may be related to the up-regulation of BDNF expression.
ABSTRACT
Objective:To evaluate the safety and effectiveness of tranexamic acid in the treatment of spontaneous intracerebral hemorrhage.Methods:Patients with spontaneous intracerebral hemorrhage admitted to the Departments of Emergency and Neurology, Nanjing Drum Tower Hospital from December 2015 to December 2018 were enrolled prospectively. The patients were randomly divided into two groups according to a random number table: tranexamic acid group and control group. All patients received conventional treatment. On this basis, 1 g of tranexamic acid injection was given to the tranexamic acid group, dissolved in 100 ml of normal saline, intravenous injection for 10 min; then 1 g of tranexamic acid was given, dissolved in 250 ml of normal saline, intravenous drip for 8 h. The control group was given an equal volume of normal saline. The main outcome measures were good outcome (defined as modified Rankin Scale score0-2) and mortality at 90 d after treatment. The secondary outcome was hematoma enlargement at 24 h after treatment and the National Institutes of Health Stroke Scale (NIHSS) score at 7 and 30 days after treatment. Platelet count and fibrinogen level were measured before treatment and 4 h after the infusion of tranexamic acid. Various adverse events were monitored.Results:A total of 150 patients were included, including 83 males (55.3%). There were 73 patients in the tranexamic acid group and 77 in the control group. There was no statistically significant difference in baseline data between the two groups. The rate of good outcome in the tranexamic acid group at 90 d was significantly higher than that in the control group (57.5% vs. 40.3%; χ2=4.476, P=0.034), while there were no significant differences in mortality rate (0% vs. 1.3%; Fisher's exact test P=1.000) and the proportion of patients with hematoma enlargement at 24 h (6.8% vs. 15.6%; χ2=2.845, P=0.092). The NIHSS score at 7 d (9.26±3.35 vs. 11.68±4.25; t=3.859, P<0.001) and at 30 d (5.45±2.52 vs. 7.38±3.28; t=4.030, P<0.001) in the tranexamic acid group were significantly lower than those of the control group. Fibrinogen in the tranexamic acid group increased significantly after treatment compared with baseline (4.20±0.56 g/L vs. 3.33±0.60 g/L; t=8.997, P<0.001), and was significantly higher than that in the control group after treatment (4.20±0.56 g/L vs. 3.30±0.55 g/L; t=9.906, P<0.001). No adverse events such as venous thromboembolism, ischemic events, and seizures were observed. Conclusion:Tranexamic acid can promote the recovery of neurological function, and improve the outcome of patients with acute spontaneous intracerebral hemorrhage, and the safety is good.
ABSTRACT
Objective To investigate the effect of cocaine and amphetamine-regulated transcript (CART ) peptides on cortical synaptic plasticity in ischemia-reperfusion (I/R ) injury mice. Methods A total of 288 healthy male specific pathogen free(SPF)grade Kunming mice aged 0 to 12 weeks were selected. They were divided into four groups:I/R group (n =81 ),I/R +CART group (n =81),sham operation group (n=63),and sham operation+CART group (n=63)according to the random number table method. A model of middle cerebral artery occlusion (MCAO)for 2 h and reperfusion was induced. Before reperfusion,the mice of the I/R+CART group were injected CART via tail vein (0. 5μg, 200μl)and the those of the sham operation+CART group were injected equal CART;repeated administration once every 24 hours. 2,3,5-Triphenyl tetrazolium chloride assay was used to detect cerebral infarction volume of the I/R group and the I/R+CART group at different time points (24 h,72 h,and day 7 )after achieving reperfusion. The transmission electron microscope was used to observe the ultrastructural changes of synapses at different time points,and the synaptic morphological parameters were analyzed quantitatively. Western blot was used to observe the expression level of postsynaptic density 95 (PSD-95)proteins in the surrounding area of cortical infarct at 72 h after reperfusion. Results (1 )Compared with the sham operation group,the number of synapses was significantly decreased in the cortical slices in the I/R group (3. 37 ± 0. 38μm2 vs. 7. 04 ± 0. 55μm2 ,2. 89 ± 0. 22μm2 vs. 6. 89 ± 0. 04μm2 ,3. 25 ± 0. 18μm2 vs. 6. 78 ± 0. 42μm2;all P0.05).Conclusion CART can reduce cerebral infarct volume of I/R in mice and improve synaptic plasticity of cortical neurons in mice after ischemic injury.
ABSTRACT
ObjectiveToinvestigatetheriskfactorsofepilepticseizuresanditseffectonclinical outcome in patients w ith cerebral venous sinus thrombosis (CVST). Methods The patients w ith CVST w ere enrol ed retrospectively. The risk factors, clinical manifestations, and imaging data w ere col ected. The data of an epileptic seizure group and a non-epileptic seizure group w ere compared. Results A total of 69 patients with CVST were enroled, including 32 (46.38%) secondary epileptic seizures. In the aspect of clinical manifestations, more patients show ed hemiplegia in the epileptic seizure group (37.50%vs.15.63%; χ2 =5.240, P=0.020). Imaging examination show ed that more patients in the epileptic seizure group presented w ith bleeding ( 29.41%vs. 10.81%; χ2 = 3.818, P= 0.047 ), more lesion involving frontal lobe (31.25%vs.10.81%; χ2 =5.008, P=0.023), and temporal lobe (43.75%vs.8.11%; χ2 =7.318, P=0.005), and the thrombosis sites w ere more common in the superior sagittal sinuses (65.63%vs.40.54%;χ2 =4.264, P=0.036). Multivariate logistic regression analysis show ed that focal neurological deficits (odds ratio 5.167, 95% confidence interval 1.993-15.764; P=0.004) and superior sagittal sinus thrombosis (odds ratio 0.126, 95% confidence interval 0.042-0.370; P=0.039) w ere the independent risk factors for patients w ith secondary epileptic seizures. There w ere no significant differences in hospital mortality (6.25%vs.2.7%; χ2 =0.512, P=0.469 ) and 90 day 90-day ful recovery rate ( defined as Barthel Index >60) (81.25%vs.86.47%; χ2 =0.346, P=0.793) betw een the epileptic seizure group and the non-epileptic seizure group. Conclusions Focal neurologic deficits and superior sagittal sinus thrombosis are the independent risk factors for secondary epileptic seizures, how ever, secondary epileptic seizures is not associ-ated w ith in-hospital mortality risk and 90-day clinical outcomes in patients w ith CVST.
ABSTRACT
BACKGROUND:Animal studies have indicated ultrasound-mediated microbubbles can significantly enhance the effect of stem cel transplantation to treat ischemic diseases. But its mechanism is stil unknown. OBJECTIVE:To explore the mechanism of ultrasound-mediated microbubbles to significantly enhance the effect of stem cel transplantation in the treatment of ischemic diseases. METHODS:Bone marrow mesenchymal stem cel s and vascular endothelial cel s of rats were cultured in vitro, and then randomized to three groups:control group with no intervention, ultrasound group exposed to ultrasound at 1 MHz, 1 W/cm2 for 90 seconds, and ultrasound-mediated microbubble group treated with 5μL liposomes ultrasound microbubbles containing fluorocarbon gases (about 2×1011/L) and ultrasound exposure at 1 MHz, 1 W/cm2 for 90 seconds. RESULTS AND CONCLUSION:Compared to the control group, ultrasound-mediated microbubbles significantly increased expressions of vascular endothelial growth factor and stromal cel-derived factor 1 in the supernatant of vascular endothelial cel s (P0.05). These findings suggest that 1 W/cm2 ultrasound-mediated microbubbles can promote vascular endothelial growth factor and stromal cel-derived factor 1 secretion by vascular endothelia cel s, and meanwhile promote CXCR4 gene expression in bone marrow mesenchymal stem cel s. This may be the mechanism of the ultrasound-mediated microbubbles enhancing homing effect of transplanted stem cel s.
ABSTRACT
Cocaine-and amphetamine-regulated transcript(CART) peptides are endogenous neurotransmitters with important roles in a number of physiological and pathological processes in vivo.Many studies suggested that CART is widely distributed in the central nervous system,and it has some central protective effects.This article reviews the recent progress in research on the protective effect of CART on cerebral ischemia and its mechanisms.