Due to the observation, lipid disorder and AT III, PS, PC factors having an important role in the formation of clots in blood vessels, cerebral infarction. This study was carried out on 123 patients with cerebral infarction and 52 normal persons. Results: The normal values of AT III, PS, PC were equal to the normal values of foreigners: AT III: 115.88719.129%; PC: 108.36019.767%; PS: 109.93725.108%. The reduction of AT III, PS, and PC had the important role in cerebral infarction, especially the reduction of PS. This relationship had statistical meaning. There was relationship between AT III and triglyceride; PS and cholesterol; PS and LDL-C in patients with cerebral infarction
Cerebral Infarction ; Lipid Metabolism Disorders

Localized, water-suppressed in vivo 'H MRS was performed to evaluated the proton metabolic alterations in patients with acute cerebral infarction.Ten brain infarction patients(six males and four females; age range 53-77) participated in this study. GE Signa 1.5-T whole-body NMI/MRS system using STEAM pulse sequence was used. Voxels were selected from the cerebral infarcted region and contralateral normal region as control in the same patient. Proton metaboliteratiosrelativetocreatine (Cr) wereobtainedusingaMa-rquartalgorithm. The specific features in the cerebral infarcted regions demonstrated a significant decrease of N-acetyl aspartate (NAA)/creatine (Cr) ratio, compared with control regions. Markedly increased lactate (Lac) level was observed in areas of cerebral infarctioln in all patients. Our preliminary study showed that NAA/Cr ratio in the infarcted regions was substanially different from that in control regions.The signal intensity of Lac may be served as a metabolic criterion that can specify acuteness of infarction, and also evaluate the therapeutic effect. It is necessary to investigate the spectral alterations in various stages of cerebral infarction for further detail analysis.
Aspartic Acid ; Brain Infarction ; Cerebral Infarction* ; Female ; Humans ; Infarction ; Lactic Acid ; Male ; Metabolism ; Protons ; Steam

BACKGROUND AND OBJECTIVES: Stroke onset is known to vary by several factors. Although it has been known that stroke may develop most frequently in the morning, its association with the type of activity has quite rarely been described. METHODS: We prospectively investigated by interview the time of and the activity during or before the onset of stroke in patients with acute cerebral infarction from Aug. 1995 to Mar. 1996. The activities were subdivided into basal metabolic rate state, sedentary, light, moderate, and heavy movements based on the caloric expenditure. RESULTS: One hundred-twenty five patients were enrolled. The time of day when ischemic stroke most frequently occurred was from 8:00 AM to noon. The type of activity was significantly associated with stroke onset in that it developed most commonly during and just after sleep or resting. The relationship between the onset of stroke and such patterns of onset time and the activity was found only in the atherothrombotic infarction, but not in the other stroke types. CONCLUSION: We demonstrated that stroke has clear diurnal variation. Our observations also suggested that the activity may be significantly associated with stroke onset. These findings may be useful for better understanding of the pathogenesis and prevention of ischemic stroke.
Basal Metabolism ; Cerebral Infarction* ; Health Expenditures ; Humans ; Infarction ; Prospective Studies ; Stroke

The purpose of this study is to investigate whether chrysin reduces cerebral ischemia-reperfusion injury(CIRI) by inhi-biting ferroptosis in rats. Male SD rats were randomly divided into a sham group, a model group, high-, medium-, and low-dose chrysin groups(200, 100, and 50 mg·kg~(-1)), and a positive drug group(Ginaton, 21.6 mg·kg~(-1)). The CIRI model was induced in rats by transient middle cerebral artery occlusion(tMCAO). The indexes were evaluated and the samples were taken 24 h after the operation. The neurological deficit score was used to detect neurological function. The 2,3,5-triphenyl tetrazolium chloride(TTC) staining was used to detect the cerebral infarction area. Hematoxylin-eosin(HE) staining and Nissl staining were used to observe the morphological structure of brain tissues. Prussian blue staining was used to observe the iron accumulation in the brain. Total iron, lipid pero-xide, and malondialdehyde in serum and brain tissues were detected by biochemical reagents. Real-time quantitative polymerase chain reaction(RT-qPCR), immunohistochemistry, and Western blot were used to detect mRNA and protein expression of solute carrier fa-mily 7 member 11(SLC7A11), transferrin receptor 1(TFR1), glutathione peroxidase 4(GPX4), acyl-CoA synthetase long chain family member 4(ACSL4), and prostaglandin-endoperoxide synthase 2(PTGS2) in brain tissues. Compared with the model group, the groups with drug intervention showed restored neurological function, decreased cerebral infarction rate, and alleviated pathological changes. The low-dose chrysin group was selected as the optimal dosing group. Compared with the model group, the chrysin groups showed reduced content of total iron, lipid peroxide, and malondialdehyde in brain tissues and serum, increased mRNA and protein expression levels of SLC7A11 and GPX4, and decreased mRNA and protein expression levels of TFR1, PTGS2, and ACSL4. Chrysin may regulate iron metabolism via regulating the related targets of ferroptosis and inhibit neuronal ferroptosis induced by CIRI.
Rats ; Male ; Animals ; Rats, Sprague-Dawley ; Ferroptosis ; Signal Transduction ; Brain Ischemia/metabolism* ; Cyclooxygenase 2/metabolism* ; RNA, Messenger ; Cerebral Infarction ; Reperfusion Injury/metabolism* ; Malondialdehyde ; Infarction, Middle Cerebral Artery

Immunohistochemistry and double immunofluorescent labeling techniques combined with confocal laser scanning microscope analysis were used to investigate the characteristic spatial induction profile of nestin following a transient middle cerebral artery occlusion in adult rat brain. The results showed that nestin was induced in ischemic core at 1 day after reperfusion. In addition to ischemic core, the expression of nestin increased in peri-ischemic I, II and III regions at 3 days and 1 week, then it decreased and narrowed along the rim of ischemic core 2 weeks after reperfusion. Double immunofluorescent labeling showed that nestin positive cells were mostly co-stained with GFAP,a astrocyte marker, in peri-ischemic I region 3 days after reperfusion. At 2 weeks, however nestin cells showed a long process and the cells double stained with nestin and NSE,a neuonal specific marker,increased in the ischemic brain. The results suggest that cerebral ischemia induces nestin expression in damaged neurons which might favor the neuroprotection against ischemic damage.
Animals ; Brain ; metabolism ; pathology ; Brain Ischemia ; metabolism ; pathology ; Immunohistochemistry ; Infarction, Middle Cerebral Artery ; metabolism ; pathology ; Nestin ; metabolism ; Neurons ; metabolism ; Rats

OBJECTIVES: Cerebral infarction is a subtype of stroke with high incidence and disability rate. Ischemia reperfusion injury (IRI) is the key point of cerebral infarction treatment. UbiA prenyltransferase domain containing 1 (UBIAD1) is a kind of enzyme with various biological functions including electron transport in mitochondrial respiratory chain, lipid metabolism, and oxidative stress which are related to IRI. The purpose of this study aims to determine the neuroprotective effects and the underlying mechanisms of UBIAD1 in cerebral IRI. METHODS: We employed oxygen-glucose deprivation/reoxygenation (OGD/R) model in mouse neuroblastoma Neuro2a (N2a) cells to mimic cerebral IRI. Lentivirus vector over-expressed UBIAD1 was transfacted into N2a cells to maintain high and stable expression of UBIAD1. In the first part of the experiment, N2a cells were divided into 5 groups: A non-OGD (N2a cells without exposure to OGD) group, groups of reoxygenation 0, 4, 12 and 24 h after 4 h of OGD, respectively. In the second part of the experiment, N2a cells were divided into 6 groups: A Con (normal cell)+non-OGD group, an EV (cell transfected with empty vector)+non-OGD group, an OE (over-expressed UBIAD1)+non-OGD group, a Con+OGD/R group, an EV+OGD/R group, and an OE+OGD/R group. In the third part, the N2a cells were divided into 8 groups: A Con+non-OGD group, an OE+non-OGD group, a Con+non-OGD+nNOS inhibitior 7-nitroindazole (7-NI) group, an OE+non-OGD+7-NI group, a Con+OGD/R group, an OE+OGD/R group, a Con+OGD/R+7-NI group, and an OE+OGD/R+7-NI group. The morphological changes of Golgi apparatus were observed under the confocal laser scanning microscope. The mRNA and protein levels of UBIAD1, secretory pathway Ca²⁺-ATPase isoform 1 (SPCA1), and NOS were determined by real-time PCR and Western blotting, respectively. Cell apoptosis rate was detected with flow cytometry; cell viability was detected with MTT assay, and NO release was determined with Griess assay. RESULTS: Compared with the non-OGD group, the expression levels of UBIAD1 mRNA and protein in N2a cells in the groups of 0, 4, 12 and 24 h reoxygenation after OGD 4 h decreased significantly (P<0.05 or P<0.01), and the longer the reoxygenation time, the more significant the reduction of UBIAD1 expression. Compared with the Con+OGD/R group and the EV+OGD/R group, mRNA and protein levels of UBIAD1 and SPCA1 were increased (P<0.05 or P<0.01), the apoptosis rate was decreased (all P<0.01), and the cell viability was increased (all P<0.01) in the OE+OGD/R group. The Golgi fragmentation was less in the OE+OGD/R group than that in the Con+ OGD/R group and the EV+OGD/R group. The mRNA and protein levels of endothelial NOS (eNOS) and neuronal NOS (nNOS) were decreased (P<0.05 or P<0.01), and the level of NO was decreased (all P<0.01) in the groups over-expressed UBIAD1 (OE+non-OGD group vs Con+non-OGD group, OE+OGD/R group vs Con+OGD/R group). The level of NO and apoptosis rate of N2a cells were decreased (all P<0.01) in the the groups pretreated with 7-NI (Con+OGD/R+7-NI group vs Con+OGD/R group, OE+OGD/R+7-NI group vs OE+OGD/R group). CONCLUSIONS UBIAD1 may exerts protective effects on OGD/R induced N2a cells by ameliorating Golgi apparatus dysfunction via the nNOS/NO pathway.
Animals ; Mice ; Cell Survival ; Cerebral Infarction ; Dimethylallyltranstransferase ; Glucose ; Lipid Metabolism ; Oxygen ; Nitric Oxide/metabolism*

This study investigated the effect of Xiaoxuming Decoction(XXMD) on the activation of astrocytes after cerebral ischemia/reperfusion(I/R) injury. The model of cerebral IR injury was established using the middle cerebral artery occlusion method. Fluorocitrate(FC), an inhibitor of astrocyte activation, was applied to inhibit astrocyte activation. Rats were randomly divided into a sham group, a model group, a XXMD group, a XXMD+FC group, and a XXMD+Vehicle group. Neurobehavioral changes at 24 hours after cerebral IR injury, cerebral infarction, histopathological changes observed through HE staining, submicroscopic structure of astrocytes observed through transmission electron microscopy, fluorescence intensity of glial fibrillary acidic protein(GFAP) and thrombospondin 1(TSP1) measured through immunofluorescence, and expression of GFAP and TSP1 in brain tissue measured through Western blot were evaluated in rats from each group. The experimental results showed that neurobehavioral scores and cerebral infarct area significantly increased in the model group. The XXMD group, the XXMD+FC group, and the XXMD+Vehicle group all alleviated neurobehavioral changes in rats. The pathological changes in the brain were evident in the model group, while the XXMD group, the XXMD+FC group, and the XXMD+Vehicle group exhibited milder cerebral IR injury in rats. The submicroscopic structure of astrocytes in the model group showed significant swelling, whereas the XXMD group, the XXMD+FC group, and XXMD+Vehicle group protected the submicroscopic structure of astrocytes. The fluorescence intensity and protein expression of GFAP and TSP1 increased in the model group compared with those in the sham group. However, the XXMD group, the XXMD+FC group, and XXMD+Vehicle group all down-regulated the expression of GFAP and TSP1. The combination of XXMD and FC showed a more pronounced effect. These results indicate that XXMD can improve cerebral IR injury, possibly by inhibiting astrocyte activation and down-regulating the expression of GFAP and TSP1.
Rats ; Animals ; Astrocytes ; Brain Ischemia/metabolism* ; Brain ; Reperfusion Injury/metabolism* ; Infarction, Middle Cerebral Artery

OBJECTIVETo investigate the correlation between plasma fibrinogen level and cerebral infarction (CI) as well as the difference of fibrinogen among subtypes of CI.

METHODSA case-controlled study was conducted with 131 cases of CI and 148 controls. Plasma fibrinogen levels were detected by the Clauss method.

RESULTSHigh fibrinogen level (3.09 +/- 0.94 g/L) was correlated with CI (OR = 2.47, 95% CI: 1.51-4.04, P < 0.005) at the onset stage of the disease. Persistent high fibrinogen level (3.14 +/- 0.81 g/L) at 6-month after stroke onset was detected and correlated with CI (OR = 4.34, 95% CI: 1.80-10.51, P = 0.001). Higher fibrinogen level was correlated with total anterior circulation infarction (TACI), partial anterior circulation infarction (PACI), and posterior circulation infarction (POCI) (OR = 4.008, P < 0.001). Higher fibrinogen level was correlated with extracranial atherosclerosis (OR = 3.220, P < 0.05, but not with intracranial atherosclerosis.

CONCLUSIONFibrinogen level may be a risk factor of CI and probably correlates with subtypes of CI and distributions of atherosclerosis.

Aged ; Atherosclerosis ; blood ; Brain Infarction ; blood ; classification ; Case-Control Studies ; Cerebral Infarction ; blood ; classification ; Female ; Fibrinogen ; metabolism ; Humans ; Infarction, Anterior Cerebral Artery ; blood ; Infarction, Posterior Cerebral Artery ; blood ; Male ; Middle Aged

OBJECTIVETo investigate the mRNA expression of monocarboxylate transporter 8 (MCT8), a thyroid hormone transport protein, in the lateral ventricle of rats with cerebral ischemia.

METHODSImmunofluorescence staining was used to observe the expression of MCT8 in the lateral ventricle of 5 normal SD rats. Another 20 adult male SD rats were randomized into 4 groups and subject to permanent ligation of both the common carotid arteries (2-vessel occlusion, 2VO) for 3 days, 2 weeks, or 5 weeks, or no ligation (control). At the end of the experiment, the transcriptional level of MCT8 in the brain tissue of the rats were detected using fluorescent quantitative PCR.

RESULTSMCT8 mRNA levels in 3-day and 2-week 2VO groups were comparable with that in the control group (P=0.909; P=0.694), but increased significantly in 5-week 2VO group compared with that in the control and 3-day 2VO groups (P=0.029; P=0.023). No significance was found in MCT8 mRNA between the 2-week and 5-week 2VO groups (P=0.065).

CONCLUSIONProlonged cerebral ischemia causes compensatory increase of MCT8 mRNA expression on the capillary endothelial cell membranes in the lateral ventricle of rats.

Animals ; Brain ; metabolism ; Brain Ischemia ; metabolism ; Cerebral Infarction ; metabolism ; Male ; Monocarboxylic Acid Transporters ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVEHypoxic-ischemic encephalopathy (HIE) is an important cause of morbidity and mortality in the neonates. Early and accurate diagnosis is helpful not only for assessing prognosis but also for making treatment decisions. The aim of this study was to explore the value of early assessment of HIE by applying the diffusion-weighted imaging (DWI) in acute (within 72 hours), subacute or chronic stages of HIE in comparison to conventional magnetic resonance imaging (MRI) in clinical practice.

METHODSImages and clinical charts of fourteen term neonates with clinically diagnosed severe hypoxic-ischemic encephalopathy treated in the NICU from January 2006 to February 2007 were retrospectively reviewed. Inclusion criteria were: term infant (37 approximately 42 weeks) and high clinical suspicion of severe HIE (low Apgar scores, need for resuscitation, metabolic acidosis, acute encephalopathy (eg, hypotonia, coma, seizures). All examinations were performed on a 3.0-T MRI system (Philips Intera Acheva Magnetom Vision) with echo-planar imaging capability with the use of a standard protocol. The imaging protocol for all the patients contained diffuse weighted images (EPI-SE, TR = 2144 ms, TE = 56 ms), T1-weighted images (TR = 389 ms; TE = 15 ms; slice thickness = 4 mm) as well as T2-weighted images (TR = 3035 ms; TE = 100 ms; slice thickness = 4 mm). The studies were first performed within 72 hours of life in these 14 consecutive patients, including both standard T1, T2-weighted image and DWI; follow-up MR studies were performed for 4 patients at the ages of 7 days, for 4 at 14 days, for another 3 at ages of both 21 days and 8 months.

RESULTSFirst inspection (on an average of 48 hours after birth): routine T1, T2-weighted images showed normal images in all patients, while diffusion images showed symmetric high intensity signal in the lateral thalami and posterior limbs of internal capsules (PLIC). Following up: on day 7, routine MRI showed both symmetric T1 prolongation and T2 slightly shortening in lateral thalami, DWI showed abnormal high signal intensity in bilateral basal ganglion (mainly in the back site of lentiform nuclei, putamen) and the cortex around central sulcus, but the previous hyperintensity in lateral thalami and PLIC disappeared. On day 14, routine MRI showed symmetric T1 prolongation, T2 shortening in bilateral thalami, lentiform nuclei and cortex around central sulus. On day 21, routine MRI showed T1 prolongation, T2 shortening in bilateral thalami and basal ganglion while previously obvious PLIC disappeared, whereas DWI showed normal images. Eight months later, deeper cerebral sulus, dilation of ventricles and widening of extracerebral space were shown.

CONCLUSIONDiffusion-weighted imaging has proved more sensitive than conventional MR imaging sequences in detecting acute cerebral infarction in adult subjects. DWI is proposed as a method for early detection of hypoxic-ischemic brain injury. In this study, DWI showed the same focus (lateral thalami and PLIC) and similar extent of the injury in these severe HIE patients in the early stage after birth (in 72 hours). The sites which showed hyperintensive signals in DWI were consistent with the foci in subsequent follow-up by routine MRI. Thus, DWI is supposed to be a technique for early assessment of the extent of hypoxic-ischemic brain injury and the prognosis in clinic. Though DWI is superior to the other imaging modalities in detecting ischemia, diffusion restriction is not necessarily indicative of permanent damage. The abnormal image on DWI may not last long. However, in chronic stage, the follow-up conventional MRI may compensate the inadequacy of DWI.

Brain ; pathology ; Cerebral Cortex ; metabolism ; Cerebral Infarction ; metabolism ; Diffusion ; Humans ; Hypoxia-Ischemia, Brain ; metabolism ; Infant ; Infant, Newborn ; Magnetic Resonance Imaging ; methods ; Stroke ; metabolism