羊脑包虫病CT、MRI影像特征

本研究旨在观察羊脑包虫病CT、MRI的特征性影像学表现.选择3只表现出脑包虫病典型症状的新疆细毛羊进行神经学检查及血常规、血清生化检查.对其中2只羊头部进行CT和MRI扫查.最后进行病理剖检,观察病理解剖变化.动物神经学检查发现动物出现眼球震颤,双侧眼睑反射、角膜反射减弱,动物的翻正反应、双侧独轮车反应存在异常;血常规...     

羊场暴发脑包虫病的诊治与防控

绵羊脑包虫病是由多头带绦虫（Taenia multiceps）的中绦期幼虫——脑多头蚴（Coenurus cerebralis）引起的一种严重危害羔羊的寄生虫病。脑多头蚴主要寄生于牛羊等反刍动物的脑和脊髓中,病畜出现一系列神经症状,最终导致死亡。介绍绵羊脑包虫病的病例情况、临床症状、病理剖解变化、诊断、手术治疗,分析发病原因,提出了针对脑包虫病的综合防控措施。     

Effects of Astragalus injection on neuronal apoptosis and expression of JNK3 in rat hippocampus after cerebral ischemia reperfusion

AIM:To investigate the effects of Astragalus injection on neuronal apoptosis and expression of c-Jun N-terminal kinase 3(JNK3) in the rat hippocampus after cerebral ischemia reperfusion. METHODS:The rat model of cerebral ischemia reperfusion was set up by a four-vessel occlusion method. The SD rats were randomly divided into 4 groups:sham operation group, cerebral ischemia reperfusion group(model group), cerebral ischemia reperfusion+Astragalus injection group(Astragalus injection group) and cerebral ischemia reperfusion+vehicle group(vehicle group). The rats in model group, Astragalus injection group and vehicle group after transient global cerebral ischemia(30 min) were then divided into 7 subgroups according to the reperfusion time of 0 h, 0.5 h, 2 h, 6 h, 24 h, 72 h and 120 h. The apoptosis of the neuron in the hippocampus was measured by the method of TUNEL staining. The expression of JNK3 at mRNA and protein levels was determined by real-time PCR and Western blotting,respectively. RESULTS:Compared with sham operation group, the number of apoptotic neurons increased in model group(P<0.05). Compared with model group, the number of apoptotic neurons decreased obviously in Astragalus injection group(P<0.05). Compared with sham operation group, the expression of JNK3 at mRNA and protein levels in the hippocampus increased obviously in model group at all time points except 120 h(P<0.05). Compared with model group, the expression of JNK3 at mRNA and protein levels in the hippocampus decreased obviously in Astragalus injection group at all time points except 120 h(P<0.05). CONCLUSION:Astragalus injection decreases neuronal apoptosis in rat hippocampus after cerebral ischemia reperfusion by inhibiting the expression of JNK3 at mRNA and protein levels.     

多头带绦虫Tm7基因的表达及间接ELISA检测方法的建立

以多头带绦虫Tm7重组蛋白为抗原,建立动物多头蚴病早期诊断方法.本研究从羊脑多头蚴原头节提取总RNA,采用RT-PCR技术首次扩增出Tm7基因的全序列,该基因的开放阅读框为207 bp,编码68个氨基酸.将此基因克隆到pET-32a(+)载体,构建重组表达质粒pET-32a-Tm7,经转化大肠杆菌BL21(DE3)后IPTG诱导表达,用SDS-PAGE和Western blot检测表达产物.以纯化后的表达蛋白作为抗原,建立检测羊脑多头蚴病抗体的重组蛋白间接ELISA方法.研究结果表明,Tm7基因在大肠杆菌中成功表达,表达产物为约27 ku的融合表达蛋白,该蛋白能识别羊脑多头蚴病阳性血清.建立的间接ELISA方法,检测敏感性可达93.3％,特异性达94.1％,研究结果表明Tm7重组蛋白可作为脑多头蚴病的诊断抗原.     

藏药五根散对缺血性脑损伤大鼠新皮质与海马中内皮素含量变化的影响

本文观察急性缺血性脑损伤饲喂藏药五根散后大鼠新皮质和海马中内皮素(ET)含量变化,旨在寻找藏药防治脑损伤的可行性。方法是用夹闭大鼠双侧颈总动脉制作急性脑缺血动物模型,然后给该大鼠喂服藏药,以放射免疫法测定脑组织(新皮质和海马)中ET含量,并与喂水组及正常组进行对比观察。结果表明:缺血性脑损伤后大鼠脑皮质与海马中ET含量明显升高,喂服藏药治疗组的ET含量比喂水组的明显下降(P<0.05)。表明缺血性脑损伤后大鼠新皮质及海马中的ET含量增加,而藏药可抑制ET合成使其含量下降,具有保护脑组织作用。     

Correlation between clinical signs of depth of anaesthesia and cerebral state index responses in dogs during induction of anaesthesia with propofol

The cerebral state index (CSI) is used for monitoring EEG and depth of anaesthesia. The objective of this study was to analyse the correlation between ocular reflexes, CSI and estimated propofol plasma concentrations (PropCP) in dogs during induction of anaesthesia with propofol.Fourteen dogs were premedicated with acepromazine 0.05 mg kg⁻¹ IM. Anaesthesia was induced with a 200 ml h⁻¹ propofol 1% constant infusion rate until loss of corneal reflex using RugLoop II software with Beths’ pharmacokinetic model to estimate PropCp.Palpebral reflex (PR) and the corneal reflex (CR) were tested every 30 s and classified as present (+) or absent (−), and eyeball position was registered as rotated ventromedialy (ERV) or centred (EC).Heart rate (HR), mean arterial pressure (MAP) and CSI values were analyzed from baseline before the beginning of propofol infusion (T0) until loss of CR; CSI and PropCp, CSI and anaesthetic planes, and PropCp and anaesthetic planes were compared using correlation analysis.PropCp reached 7.65 ± 2.1 μg ml⁻¹ at the end of the study. CSI values at T0 were 89.2 ± 3.8. Based on the observation of ocular reflexes and eyeball position, it was possible to define five anaesthetic planes: A (superficial) to E (deep), being A (PR+/CR+/EC), B (PR+/ERV/CR+), C (PR−/ERV/CR+), D (PR−/EC/CR+) and E (PR−/EC/CR−). There was a significant correlation between PropCp and the anaesthetic planes (R = 0,861; P < 0.01). No significant correlation was observed between CSI and the anaesthetic planes or between CSI and PropCp. MAP decreased significantly from T0 until loss of corneal reflex (from 98 ± 14 mmHg to 82 ± 12 mmHg); HR did not change significantly (from 101 ± 30 bpm to 113 ± 16 bpm).The CSI monitoring was not consistent with the clinical observations observed in the different stages of depth anaesthesia. This could limit the use of CSI for monitoring depth of anaesthesia with propofol.     

Polymicrogyria in Standard Poodles

Background: Polymicrogyria is a disorder of cerebrocortical migration resulting in increased numbers of small, disorganized gyri. This disorder occurs in Standard Poodles and in cattle.
Objectives: To describe the clinical, electroencephalographic, imaging, and histopathologic features in poodles with polymicrogyria.
Animals: Five Standard Poodles with histologically confirmed polymicrogyria.
Methods: Retrospective case series. Cases were obtained by personal communication with 1 of 2 authors (TJVW, DPO).
Results: All dogs had cortical blindness and other neurologic abnormalities including gait and behavioral changes. Magnetic resonance imaging of 3 dogs showed multiple disorganized gyri, which were especially apparent on T2-weighted dorsal plane images. Electroencephalogram (EEG) of 1 dog revealed epileptiform discharges, including both spike and spike and wave discharges with voltage maximum potentials over the parietal/occipital region. The EEG supported that the repetitive behavior displayed by the dog was a complex partial motor seizure. One dog had concurrent hydrocephalus. All dogs had occipital lobe involvement and 2 dogs had involvement of other lobes.
Clinical Importance: The cases presented here demonstrate a larger age range (7 weeks to 5 years) and a decreased frequency of associated hydrocephalus when compared with the previous report.     

Effects of peripheral-type benzodiazepine receptors in platelet membrane on patients with depression after first attack of cerebral infarction

AIM：To evaluate the changes of peripheral-type benzodiazepine receptors (PBRs) in platelet membrane in post-stroke depression (PSD) patients and to investigate the effects of PBRs on PSD. METHODS：Forty-three patients with PSD, fifty-nine patients with first-ever cerebral infarction and fifty-six healthy volunteers participated in this study. Platelet membrane in venous blood was prepared. Binding assay of the radioactive PBRs antagonist ［3H］PK11195 to platelet membrane was performed. RESULTS：A significant difference of ［3H］PK11195 binding was found among the 3 groups (P<0.01). Compared with the healthy volunteers ［(298.2±25.1） pmol/(g protein)］, a highly significant increase in ［3H］PK11195 binding was observed in platelet membrane in the patients with first attack of cerebral infarction ［(1 410.8±41.4） pmol/(g protein), P<0.01］. Compared with the patients with first attack of cerebral infarction, a significant reduction in ［3H］PK11195 binding was detected in platelet membrane in the patients with PSD ［(361.7±30.6) pmol/(g protein), P<0.01］. In the patients with PSD, no significant difference of ［3H］PK11195 binding was found between men and women (P>0.05). ［3H］PK11195 binding was related to the score of Hamilton depression rating scale (r=-0.44, P<0.01) but not to the duration of cerebral infarction (r=0.27,P>0.05). CONCLUSION:PBRs binding activity in platelet membrane decreases in the patients with PSD and affects the degree of depression.     

Selective up-regulation of Toll-like receptor 9 in mouse microglia after cerebral infarction

AIM：To observe the expression of Toll-like receptor 9 (TLR9) and the distribution of TLR9 in the neurons and glial cells after cerebral infarction. METHODS：With the intraluminal filament method, middle cerebral artery occlusion (MCAO) model of C57 mice was established, and the filament was removed to begin reperfusion 90 min later. A sham-operated group was set up as a control. At 6 h, 3 d, 7 d or 14 d after reperfusion, the mice were randomly killed to prepare brain coronal cryosections (n=3). The level of TLR9 expression and the distribution of TLR9 in the neurons and glial cells were detected by immunofluorescent staining. RESULTS：The level of TLR9 increased significantly in transitional peri-infarct tissues over time and was constantly higher than that in the contralateral and sham-operated ones. Only a few scattered TLR9 staining was found inside the neurons during the whole process. The percentage of TLR9-positive neurons showed no significant difference among groups and time points. Activated microglia aggregated in transitional peri-infarct tissues, with intracellular TLR9 staining from scattered tiny dots to clustered coarse particles. Meanwhile, the percentage of TLR9-positive microglia increased at the beginning and later decreased with time, and was significantly higher than that in the contralateral and sham-operated ones. No TLR9 expression was found in astrocytes or oligodendrocytes. CONCLUSION：TLR9 is triggered in microglia after cerebral infarction in the CNS, while the neurons maintain inherent expression of TLR9. Besides, there is no evidence to support the expression of TLR9 in the astrocytes and oligodendrocytes.