Effect of Aerobic Exercise on Behavioral Function in Rats with Cerebral Small Vessel Disease / 中国康复理论与实践

Objective:To explore the effect of aerobic exercise on behavioral function in rats with cerebral small vessel disease and its mechanism. Methods:Eight-week-old male Sprague-Dawley rats were randomly divided into sham group (n = 16), model group (n = 16) and swimming group (n = 16). The model was developed with bilateral common carotid artery ligation. They were assessed with burrowing test after four weeks of swimming exercise. The levels of brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) protein in hippocampus were detected with Western blotting. The development of dendrites and synaptic spines in hippocampal neurons was observed with Golgi staining. The expression of Ki67, doublecortin (DCX) and Neun in hippocampal dentate gyrus was detected with immunofluorescence. Results:Compared with the model group, the burrowing ability improved in the swimming group (P < 0.05), with increase of levels of BDNF and TrkB in hippocampus (P < 0.05), Ki67/DCX and Neun positive cells in hippocampal dentate gyrus (P < 0.05), and extension of dendrites and length of synaptic spine in hippocampal neurons (P < 0.05). Conclusion:Aerobic exercise may promote the proliferation and differentiation of hippocampal neurons through BDNF/TrkB signaling pathway, expression of Ki67/DCX and Neun and development of hippocampal neurons, to improve behavioral function in rats with cerebral small vessel disease.

Influence of Sleep Deprivation on Blood-brain Barrier in Rats / 中国康复理论与实践

Objective:To investigate the influence of sleep deprivation (SD) on blood-brain barrier in adult male rats. Methods:A total of 90 healthy male Sprague-Dawley rats were randomly divided into SD group, SD and recovery (SDR) group and control (K) group. SD group and SDR group were continuously deprived of sleep for five days by horizontal table, and then, SDR group were fed normally for two days after SD. K group accepted no intervention. The leakage of Evens Blue (EB) in brain was observed after EB perfusion. The expression of zonula occludens-1 (ZO-1), Occluding, Claudin-5, Bax/BCL-2, P53 and caspase-3 in the cortex was detected with Western blotting. The apoptosis of neurons and endothelial cells in cortex was observed with immunofluorescence staining. Results:In SD group, EB was observed in multiple cerebral lobe and extensive cortex, and it was also observed in SDR group in a milder way, but not observed in K group. The expression of P53, Caspase-3, Bax/BCL-2 in the cerebral cortex was the most in SD group, and the least in K group; while the expression of ZO-1, Occluding and Claudin-5 was the least in SD group, and the most in K group, and it was in-between in SDR group (F > 39.915, P < 0.001). The CD31 and NeuN positive cells decreased in cortex were the least in SD group, and the most in K group, while the TUNEL positive cells were the most in SD group, and the least in K group, and the levels of CD31, NeuN and TUNEL positive cells were in-between in SDR group (F > 142.056, P < 0.001). Conclusion:SD may lead to dysfunction of permeability of blood-brain barrier, while decrease expression of tight junction protein, and increase apoptosis of neurons in rats to reduce the neurons and endothelial cells in cerebral cortex. Sleep recovery may partly alleviate these impacts.

Prenatal diagnosis of fetal urinary abnormalities and microdeletion on chromosome 1q21.1 / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate genetic etiology of fetal urinary abnormalities with array-based comparative genomic hycridization(array-CGH).</p><p><b>METHODS</b>Thirty-two fetuses with variable urinary abnormalities but normal karyotyping by conventional cytogenetic technique were selected. DNA from the fetuses and their parents samples were prepared and hybridization with Affymetrix cytogenetic 2.7M arrays by follwing the manufacture's standard protocol. The data were analyzed by special CHAS software packages.</p><p><b>RESULTS</b>By using array-CGH detection, genomic imbalanced copy number variations (CNVs) were identified in night fetuses(28%), four out of night CNVs were inherited from parental samples; two were indicated to be benign variants(6%) in the database; and the other three CNVs (9%) were all de novo adjacent microdeletions and microduplication mapping on to common chromosome 1q21.1 region, within which was genitourinaty system function associated gene PDZK1.</p><p><b>CONCLUSION</b>The incidence of genomic unbalanced variations in fetuses with congenital urinary malformations is approximately 28%, including about 9% pathogenic variations. Copy number variations (CNVs) of chromosome 1q21.1 region are associated with congenital urinary malformations which may be due to haploinsufficiency or overexpression of PDZK1 gene.</p>

The quantitative analysis of Ub and UbE1 in focus of traumatic epilepsy / 法医学杂志

OBJECTIVE@#To study the expression of ubiquitin proteasome system (UPS) in the traumatic epilepsy pathogenesis and its value in traumatic epilepsy by quantitative analysis.@*METHODS@#Fifteen specimens from human epileptic temporal cortex from PTE were collected as the PTE group. Fifteen specimens from non-PTE were collected as the non-PTE group. Fifteen normal cerebral cortex specimens died from acute traffic accident were collected as the control group. The expression of mRNA and protein of Ub and UbE1 were detected by RT-PCR and Western blot. Statistical analysis was used to compare the data between three groups.@*RESULTS@#The expression of mRNA and protein of Ub and UbE1 were the following order: PTE group(high), non-PTE group(middle) and control group(low).@*CONCLUSION@#The study confirms that UPS is up-regulated in the epilepsy's focus, especially in traumatic epilepsy. The activation of UPS may be an important pathological change in neurons in pathogenesis of traumatic epilepsy.

Morphology changes of ubiquitin-proteasome system in traumatic epilepsy / 法医学杂志

OBJECTIVE@#To investigate the value of ubiquitin(Ub) and ubiquitin-activating enzymel(UbE1) for the appraisement of post traumatic epilepsy (PTE).@*METHODS@#Fifteen specimens from human epileptic temporal cortex originating from PTE were collected as the PTE group. Fifteen specimens from non-PTE were collected as the non-PTE group. Meanwhile, 15 normal cerebral cortex specimens from people dead from acute traffic accident were collected as the control groups. Observe morphology changes of each group with HE, then with immunohistochemistry of Ub and UbE1.@*RESULTS@#Compared to the control group, morphology changes of neuron quantity reduction, neuron denaturation and so on were observed both in the PTE group and the non-PTE group under HE, especially in the PTE group. Ub and UbE1 mainly expressed in the nucleus and cytoplasm of the neurons in epilepsy spot without extracellular expression. The expression of Ub and UbE1 is PTE group > non-PTE group > control group (P < 0.05).@*CONCLUSIONS@#The neuron denaturation are one of the main pathology changes of epilepsy, and it is more obvious in the PTE group. Immunohistochemistry of Ub and UbE1 may be more helpful to distinguish PTE and non-PTE than HE staining.