2.Roles of astrocytes in cerebral infarction and related therapeutic strategies.
Jianyu YE ; Ziyu SUN ; Weiwei HU
Journal of Zhejiang University. Medical sciences 2018;47(5):493-498
Astrocytes are the most abundant cells in the central nervous system and play significant roles in normal brain. With cerebral infarction, astrocytes are activated as reactive astrocytes and form glial scars, which play an essential part in brain injury. According to their roles in neuroprotection after cerebral infarction, regulation of scar formation, nerve regeneration, maintenance of blood-brain barrier, promotion of angiogenesis and immune response, scholars have proposed a variety of therapeutic strategies based on targeting astrocytes. This article reviews the research progress on the changes in astrocyte signaling pathways before and after cerebral infarction and the related therapeutic strategies.
Astrocytes
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Cerebral Infarction
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physiopathology
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therapy
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Humans
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Neuroglia
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pathology
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Signal Transduction
4.Impact of obstructive sleep apnea-hypopnea syndrome on cerebral microbleeds in patients with cerebral infarction.
Jiewen XU ; Liying DENG ; Xueliang ZOU ; Hao LIU ; Ye YU ; Yongmin DING
Journal of Southern Medical University 2012;32(9):1362-1365
OBJECTIVETo investigate the impact of obstructive sleep apnea-hypopnea syndrome (OSAHS) on cerebral microbleeds (CMBs) in patients with cerebral infarction.
METHODSConsecutive patients with acute cerebral infarction who had cerebral microbleeds shown by susceptibility-weighted imaging (SWI) were enrolled to undergo polysomnography (PSG). The patients were divided into two groups, namely non-OSAHS group with apnea-hypopnea index (AHI) less than 5 and OSAHS group with greater AHI, and the clinical and radiological features of cerebral microbleeds were compared between them.
RESULTSForty-nine patients were enrolled in this study, including 27 (55.1%) with both cerebral infarction and OSAHS and 22 (44.9%) with cerebral infarction but not OSAHS. A comparison of the risk factors showed that hypertension, a smoking history, and a history of stroke were more prevalent in patients with OSAHS than in those without OSAHS (P<0.05). The incidences of subclinical stroke in OSAHS and non-OSAHS patients were 37.0% (10/27) and 9.0% (2/22) (P<0.05), respectively. Neurological imaging revealed a greater number of cerebral microbleeds in OSAHS group than in non-OSAHS group (P<0.05). In OSAHS patients, 77.8% of the microbleeds were distributed in cortical-subcortical areas, 55.6% in the basal ganglia area, and 25.9% in the infratentorial area, as compared to the percentages of 50.0%, 40.9% and 50.0% in non-OSAHS patients, respectively (P<0.05). In OSAHS patients, 40.7% also had leukoaraiosis, and 48.1% had two or more causes, as compared to the percentages of 13.6% and 18.2% in non-OSAHS patients, respectively (P<0.05).
CONCLUSIONSOSAHS can be a risk factor for cerebral microbleeds. Patients with both cerebral infarction and OSAHS tend to have greater and more extensive lesions of cerebral microbleeds, more complicated cause of the disease, and a grater likeliness of stroke recurrence.
Aged ; Cerebral Hemorrhage ; etiology ; pathology ; Cerebral Infarction ; pathology ; Female ; Humans ; Male ; Middle Aged ; Risk Factors ; Sleep Apnea, Obstructive ; complications ; pathology
5.On the quantitative analysis of focal ischemic cerebral infarction by TTC staining.
Chunyan FENG ; Xiaonong FAN ; Chunhong ZHANG ; Xuemin SHI
Journal of Biomedical Engineering 2009;26(6):1363-1366
It is known that ischemic cerebrovascular disease is causing enormous harm to human health on account of the resultant high morbidity and disability rate. In this connexion, the anticipated target is to control the size of focal ischemic cerebral infarction, which is also an important method for judgment of therapeutic efficacy. The key question is to survey the size accurately and objectively; at the same time, the quantitative analysis of focal ischemic cerebral infarction is the pivotal question affecting the experiment conclusion and the reliability level. In this paper are introduced and summarized the methods being recently and commonly used in survey and computation, and the studies made on quantitative analysis of focal ischemic cerebral infarction by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining method. Also are summarized the principles of dyeing in TTC method, the preparatory work, and the commonly used method of surveying and computation. It is the intent of this review to provide relevant data and suggestion for research workers.
Animals
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Brain Ischemia
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pathology
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Cerebral Infarction
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pathology
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Coloring Agents
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Humans
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Reperfusion Injury
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pathology
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Tetrazolium Salts
6.Lenticulostriate Artery Involvement is Predictive of Poor Outcomes in Superficial Middle Cerebral Artery Territory Infarction.
Kijeong LEE ; Eun Hye KIM ; Dongbeom SONG ; Young Dae KIM ; Hyo Suk NAM ; Hye Sun LEE ; Ji Hoe HEO
Yonsei Medical Journal 2017;58(1):123-130
PURPOSE: Patients with superficial middle cerebral artery (MCA) territory infarction may have concomitant lenticulostriate artery (LSA) territory infarction. We investigated the mechanisms thereof and the outcomes of patients with superficial MCA territory infarction according to the presence or absence of LSA involvement. MATERIALS AND METHODS: Consecutive patients with first-ever infarction in the unilateral superficial MCA territory were included in this study. They were divided into the superficial MCA only (SM) group and the superficial MCA plus LSA (SM+L) group. RESULTS: Of the 398 patients, 84 patients (21.1%) had LSA involvement (SM+L group). The SM+L group more frequently had significant stenosis of the proximal MCA or carotid artery and high-risk cardioembolic sources. Stroke severity and outcomes were remarkably different between the groups. The SM+L group showed more severe neurologic deficits (National Institute of Health Stroke Scale score 10.8±7.1 vs. 4.0±5.0, p<0.001) and larger infarct in the superficial MCA territory (40.8±62.6 cm³ vs. 10.8±21.8 cm³, p<0.001) than the SM group. A poor functional outcome (mRS >2) at 3 months was more common in the SM+L group (64.3% vs. 15.9%, p<0.001). During a mean follow-up of 26 months, 67 patients died. All-cause (hazard ratio, 2.246) and stroke (hazard ratio, 9.193) mortalities were higher in the SM+L group than the SM group. In multivariate analyses, LSA involvement was an independent predictor of poor functional outcomes and stroke mortality. CONCLUSION: LSA territory involvement is predictive of poor long-term outcomes in patients with superficial MCA territory infarction.
Carotid Stenosis/mortality/pathology
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Constriction, Pathologic/pathology
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Female
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Humans
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Infarction, Middle Cerebral Artery/mortality/*pathology
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Male
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Middle Cerebral Artery/*pathology
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Multivariate Analysis
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Severity of Illness Index
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Stroke/mortality/pathology
7.Herpes zoster ophthalmicus and delayed contralateral hemiparesis.
Ki Bum SUNG ; Seung Hyun KIM ; Ju Han KIM ; Kyung Cheon CHUNG ; Myung Ho KIM
Journal of Korean Medical Science 1988;3(2):79-82
Central nervous system is often involved by herpes zoster but it is very rarely seen that contralateral hemiparesis or hemiplegia developed after herpes zoster ophthalmicus. We report a case of herpes zoster ophthalmicus followed by the delayed contralateral hemiparesis. A 33-year-old man developed acute cerebral infarction and resultant right hemiparesis 44 days after herpes zoster ophthalmicus in the left side. Brain CT disclosed hypodense area in the left basal ganglia. Cerebral angiography revealed segmental narrowing of M1 portion of the right middle cerebral artery.
Adult
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Cerebral Angiography
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Cerebral Arteries/pathology
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Cerebral Infarction/*etiology/radiography
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Dominance, Cerebral
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Hemiplegia/*etiology
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Herpes Zoster Ophthalmicus/*complications
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Humans
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Male
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Tomography, X-Ray Computed
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Vasculitis/etiology
9.The effects of peripheral leukocytes on the hippocampal neuronal changes in transient global ischemia and unilateral cerebral hemispheric infarction.
Hyang Won LEE ; Heasoo KOO ; Kyung Gyu CHOI ; Kee Duk PARK ; Byung Chul LEE
Journal of Korean Medical Science 1999;14(3):304-314
The participation of activated leukocytes and subsequent production of chemical mediators has been well accepted in the pathophysiology of hypoxic-ischemic injury. This study was performed to see the effects of leukocytes on hippocampal neuronal damage in transient global ischemia induced by 10-min occlusion of bilateral common carotid arteries (CCAs) with reperfusion for various times, and in complete unilateral ischemia induced by 24-hr ligation of left CCA. Leukopenia was induced by intraperitoneal injection of cyclophosphamide for 4 days. The results showed that hippocampal neuronal damages were worse at 6-hr reperfusion in leukopenic experimental group than in the control group. In comparison, 24-hr and 3-day reperfusion leukopenic groups showed less numbers of damaged neurons and milder changes. The 5-day reperfusion group showed inconsistent changes. Unilateral CCA occlusion showed extensive infarction in 83.3% of gerbils in the control group, compared to 25% of gerbils in the experimental group (p<0.05). These results strongly suggest that the number of peripheral leukocytes were closely related to the development of delayed neuronal damage of hippocampus in transient global ischemia and the incidence of infarction induced by 24-hr unilateral CCA ligation.
Animal
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Cerebral Infarction/pathology*
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Female
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Gerbillinae
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Hippocampus/pathology*
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Leukocyte Count
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Leukocytes/physiology*
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Male
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Neurons/pathology*
;
Reperfusion Injury
10.The expression of nestin in ischemia-injured brain of adult rat.
Peng-Chong LIU ; Shi-Duo LU ; Ya-Lin HUANG ; Feng-Yan SUN
Acta Physiologica Sinica 2002;54(4):294-299
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
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Brain
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metabolism
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pathology
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Brain Ischemia
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metabolism
;
pathology
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Immunohistochemistry
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Infarction, Middle Cerebral Artery
;
metabolism
;
pathology
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Nestin
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metabolism
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Neurons
;
metabolism
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Rats