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Objective:To explore the predictive value of the recurrence risk estimator at 90-days(RRE-90) score combined with lipoprotein-associated phospholipase A2 (Lp-PLA2) and high sensitivity C-reactive protein(hs-CRP) in the recurrence risk of acute atherosclerotic cerebral infarction.Methods:Totally 400 patients with acute atherosclerotic cerebral infarction who were hospitalized for the first time in neurology department were followed up for 90 days.However, 8 cases were lost and 392 cases were included finally.According to recurrence or not, 64 cases were divided into recurrence group and 328 cases into non-recurrence group.The RRE-90 score was applied to all the participants and the levels of Lp-PLA2 was detected by enzyme-linked immunosorbent assay, the levels of hs-CRP was detected by immunoturbidimetry.The ROC curve was used to analyze the predictive value of RRE-90 score combined with Lp-PLA2 and hs-CRP for the recurrence risk of acute cerebral infarction.Results:Compared with the non-recurrence group(RRE-90: (3.07±1.01)score, Lp-PLA2: (103.53±8.11)μg/L, hs-CRP: (4.07±1.48)mg/L), the levels of (RRE-90 score: (4.11±0.78)score, Lp-PLA2: (121.52±13.95)μg/L, hs-CRP: (12.40±2.46) mg/L)in the recurrence group of cerebral infarction were significantly higher ( P<0.05, P<0.01). Compared with RRE-90 score (0.705), Lp-PLA2 (0.697), hs-CRP (0.622), RRE-90 score combined with Lp-PLA2 (0.752), RRE-90 score combined with hs-CRP (0.746), RRE-90 score combined with Lp-PLA2 and hs-CRP (0.782) had the largest area under the curve for predicting recurrence of cerebral infarction within 90 days, with statistical significance( P<0.05), sensitivity was 87.8%, specificity was 89.6%. Conclusion:RRE-90 score combined with Lp-PLA2 and hs-CRP detection can further improve the accuracy of predicting recurrence within 90 days in patients with cerebral atherosclerotic infarction, and the predictive value is high.
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Objective To explore the influencing factors of the collateral circulation formation in patients with acute cerebral infarction.Methods Three hundred and fifty-two patients with acute cerebral infarction were included in this study,the clinical date of their head and neck 256 slice spiral CT angiography (CTA)examination was analyzed.According to the formation of collateral circulation in the head and neck CTA imaging results,it is divided into the collateral circulation group and the non-collateral circulation group.The clinical data of the two groups were compared.The influencing factors of the formation of collateral circulation in patients with acute cerebral infarction were analyzed by single factor analysis and multivariate logistic regression analysis.Results (1)In 352 cases of acute cerebral infarction,197 cases(56.0%)had collaterals,155 cases (44.0%)had none collateral.(2)Single factor analysis showed that age(t=-2.860,P=0.004),hypertension combined with diabetes(χ2 = 10.709,P= 0.001),history of TIA(χ2 = 4.626,P= 0.034),low density lipoprotein(t=-2.176,P=0.030),high homocysteine(t=2.885,P=0.004),cerebral vascular stenosis(Z=-5.936,P=0.000),posterior circular lesions(χ2=8.548,P=0.004)were the influencing factors in the formation of collateral circulation.(3)Multivariate Logistic regression analysis showed that old age(OR=1.031;95%CI=1.008-1.054;P=0.007),hypertension combined with diabetes(OR= 2.009;95%CI=1.159-3.482;P=0.013),high homocysteine(OR=1.023;95%CI,1.005-1.041;P=0.014),circular lesions(OR=1.727;95%CI=1.063-2.804;P=0.027)were relatively independent risk factors in acute cerebral infarction patients with none circulation,the degree of cerebral vascular stenosis(OR=0.507;95%CI=0.389-0.661;P=0.000),low density lipoprotein(OR=0.723;95%CI=0.532-0.982;P=0.038)served as protective factor.Conclusion Old age,hypertension combined with diabetes,high homocysteine and posterior circulation lesions are risk factors for the formation of collateral circulation in patients with acute cerebral infarction,cerebral vascular stenosis degree and low density lipoprotein can promote the formation of collateral circulation.
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Objective To observe the effects of autophagy on the expression of synaptic plasticity related protein, growth-associated pro-tein-43 (GAP-43) and microtubule associated protein-2 (MAP-2), in CA1 area of hippocampus of vascular dementia rats. Methods Nine-ty-six healthy male Sprague-Dawley rats were randomly divided into sham group, vascular dementia model group (VD group), autophagy in-hibitor 3-methyl adenine preconditioning group (3-MA group) and autophagy agonist rapamycin preconditioning group (Rap group). Each group was divided randomly into subgroups of one week, two weeks, four weeks and eight weeks after modeling, six rats in each group. The vascular dementia rat model was established with modified Pulsineli's four-vessel occlusion. The expression of GAP-43 and MAP-2 in CA1 area of hippocampus were detected with immunohistochemistry. Results Compared with the sham group, the expression of GAP-43 protein increased, and the expression of MAP-2 protein decreased at every time point in VD group (P<0.01). Compared with VD group, the expres-sion of both GAP-43 and MAP-2 increased in 3-MA group (P<0.05), and decreased in Rap group (P<0.05). Conclusion Autophagy may in-hibit the expression of synaptic plasticity related protein, GAP-43 and MAP-2, in CA1 area of hippocampus in vascular dementia rats, indi-cating inhibition of autophagy may promote synaptic remodeling.
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@#Objective To observe the expression of microtubule-associated protein 1 light chain 3 II (LC3II) and microtubule-associated protein 2 (MAP-2) in CA1 area of hippocampus in vascular dementia rats. Methods 48 Sprague-Dawley rats were randomly divided into sham group and model group. Meanwhile, each group was further divided into 1, 2, 4 and 8 weeks subgroups (n=6). Vascular dementia model was established by blocking four vessels. The expressions of LC3II and MAP-2 protein were detected with immunohistochemistry in the CA1 area of hippocampus. Results The expression of LC3II significantly increased, and the expression of MAP-2 decreased in the model group compared with the sham group at every time point (P<0.001). The expression of LC3II was negatively correlated with MAP-2 at every time point in the model group (r=-0.723, P<0.05). Conclusion It may play an important role for the occurrence and development of vascular dementia that the expression of LC3II increased and MAP-2 descreased in CA1 area of hippocampus in rats.
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[Abstract ] Objective The purpose of this study was to observe the effects of dl-3n-butylphthalide (NBP) sodium chloride injection post-processing on the expressions of X-inhibitor of apoptosis (XIAP) and Bcl-2/adenovirus E1B19kDa interacting protein 3 (BNIP3) in the hippocampus CA1 neurons of focal cerebral ischemia reperfusion (IR) rats, and to investigate the brain-protection mechanisms of NBP. Methods A total of65 adult male Sprague-Dawley rats were divided into five groups of equal number, sham op-eration, IR, and low-,medium -and high-dose NBP, according to the random number table. The IR models were established by modified ligation of the middle cerebral artery.The animals in the NBP groups received intra-abdominal injection of NBP at 2, 4, and 6 mg/kg, re-spectively.All the rats were sacrificed at 24 hours after modeling,neurological scores obtained by Zea Longa, the volume of infarction measured by TTC staining, the number of apoptotic cells counted by TUNEL, and the expressions of XIAP and BNIP3 detected by immunohistochemistry and real-time PCR. Results The neural function defect scores were markedly lower in low-, medium-and high-dose NBP groups than in IR model rats (P<0.05), with statis-tically significant differences among the three dose groups (P<0.05).The volume of infarction was remarkably higher in the low-dose than in the medium-and high-dose NBP groups (P<0.05).The number of apoptotic cells in the hippocampus CA1 neurons was de-creased in the NBP groups as compared with the IR models (P<0.05).The XIAP-and BNIP3-positive cells were significantly in-creased in the IR model rats as compared with the sham operation group ([22.31 ±0.94] and [60.13 ±2.59]/HP vs [3.07 ±1.43] and [5.78 ±0.44]/HP, P<0.05).In comparison with the IR models, the NBP-treated rats showed a progressively increased number of XIAP-positive cells in low-, medium-, and high-dose groups ([28.70 ±1.18], [32.79 ±0.88], and [37.01 ±1.24]/HP) (P<0.05) but a decreased number of BNIP3-positive cells in the three dose groups ([52.07 ±1.02], [40.30 ±2.00], and [31.04 ± 0.43]/HP) (P<0.05).Similarly, the expression of XIAP mRNA was up-regulated while that of BNIP3 mRNA down-regulated in the NBP treatment groups as compared with the IR model rats, both in a dose-dependent manner (P<0.05). Conclusion NBP post-processing has a neuroprotective effect on IR rats, which is associated with its impact on the expressions of XIAP and BNIP3.
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Objective To observe the expression of microtubule-associated protein 1 light chain 3 II (LC3II) and microtubule-associated protein 2 (MAP-2) in CA1 area of hippocampus in vascular dementia rats. Methods 48 Sprague-Dawley rats were randomly divided into sham group and model group. Meanwhile, each group was further divided into 1, 2, 4 and 8 weeks subgroups (n=6). Vascular dementia mod-el was established by blocking four vessels. The expressions of LC3II and MAP-2 protein were detected with immunohistochemistry in the CA1 area of hippocampus. Results The expression of LC3II significantly increased, and the expression of MAP-2 decreased in the model group compared with the sham group at every time point (P<0.001). The expression of LC3II was negatively correlated with MAP-2 at ev-ery time point in the model group (r=-0.723, P<0.05). Conclusion It may play an important role for the occurrence and development of vas-cular dementia that the expression of LC3II increased and MAP-2 descreased in CA1 area of hippocampus in rats.
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This study was aimed to explore the methodology regarding culture, proliferation and purification of adipose-derived stromal cells (ADSCs), and to study their biological characteristics. ADSCs were obtained using type I collagenase digestion method. Cell growth was observed, and cell viability were detected under different digestion period by MTT. The ADSCs were then identified and induced. The results showed that adherent cells digested by type I collagenase for 60 min had a strong proliferation capability. After the induction of different inducers these adherent cells could differentiate into nerve cells and fat cells. The best digestion period was proved to be of 60 minutes in the experiment. The results indicate that stem cells with multilineage differentiation ability could be separated from adipose tissue, namely ADSCs.
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Adipocytes , Cell Biology , Adipose Tissue , Cell Biology , Cell Differentiation , Cell Proliferation , Cells, Cultured , Neurons , Cell Biology , Primary Cell Culture , Stem Cells , Cell Biology , Stromal Cells , Cell BiologyABSTRACT
To investigate the association of HLA-A0205 and HLA-A30 with latent autoimmune diabetes mellius in adults (LADA) in Chengdu Hans, 121 subjects (41 cases of LADA, 40 cases of T2DM, and 40 normal controls) were enrolled in the study. The frequencies of HLA-A0205 and HLA-A30 were determined by nested PCR-SSP and direct sequencing, respectively. The allele frequencies of patient groups and of normal controls were compared by chi-square test using SPSS 11.0 (alpha = 0.05). Hardy-Weinberg equilibrium was tested with use of software HWE (alpha = 0.05). Data from the subjects showed: HLA-A0205 was present in 1 patient with LADA and in 1 normal control (2.44% and 2.5%, respectively), HLA-A30 was present in 2 patients with LADA, in 2 patients with T2DM and in 1 normal control (4.87%, 5.0% and 2.5%, respectively). There was no statistically significant difference between the allele frequencies of the three groups. These results suggest that HLA-A0205, HLA-A30 may not be related to LADA in Chengdu Hans. Yet, further studies with larger sample size may be needed to warrant this conclusion.