Dyskinesia is the most common motor complication in advanced Parkinson's Disease (PD) and has a severe impact on daily life. But the mechanism of dyskinesia is still poorly understood. This study aims to explore risk factors for disabling dyskinesia in PD and further analyze the Vesicular Monoamine Transporter 2 (VMAT2) distribution (labeled with 18F-AV133) in the corpus striatum and the 18F-fluorodeoxyglucose (18F-FDG) metabolism of different brain regions by PET-CT.This is a cross-sectional study involving 135 PD patients. They were divided into disabling dyskinesia group (DD group, N=22) and non-dyskinesia group (ND group, N=113). All the patients were agreed to undergo PET-CT scans. Clinical data were analyzed between two groups by using multivariate logistic regression analysis, and risk factors for disabling dyskinesia were then determined. The standard uptake value ratios (SUVr) of 18F-AV133 in the corpus striatum and the 18F-FDG metabolism of different brain regions were identified and calculated by the software.16.3% patients have disabling dyskinesia. DD group were more likely to have longer Disease Duration, higher Hoehn-Yahr degree, more severe clinic symptoms, more frequent sleep behavior disorder, and higher levodopa dose equivalency than ND group (P < 0.05). After adjusting confounding factors by multivariate logistic regression, DD group had longer PD duration and high levodopa dose equivalency compared with ND group (P < 0.05). There is no significant difference between the VMAT2 distribution (labeled with 18F- AV133) in the putamen and caudate between two groups. And the 18F-FDG metabolic changes in cortical and subcortical regions did not show a significant difference between the two groups either (P > 0.05).Long PD duration and high levodopa dose equivalency were two independent risk factors for disabling dyskinesia in PD patients. Compared to non-dyskinesia PD patients, there was no significant dopamine decline of the nigrostriatal system in disabling dyskinesia PD patients. Activities of different brain regions were not different between the two groups by 18F-FDG PETCT.
Objective To explore radiotoxicity of 125I labeled nerve growth factor (125I-NGF) in U251. Methods Absorbance values of U251 treated with 18.5, 37.0, 74.0, 148.0, 296.0, 592.0,1184. 0, 1480. 0, 1850. 0, 2590. 0, 3330. 0, 3700. 0 kBq/ml 125I-NGF were detected by MTT assay. The corresponding minimum concentration of 125I-NGF tending to the minimum absorbance value was selected as minimum effective concentration, and was adopted in follow-up experiments. Plate colony-forming assay was adopted to compare the proliferation ability of cells treated with complete culture medium, 592 kBq/ml Na125I, 1 mg/L NGF and 592 kBq/ml 125I-NGF. Distribution of silver particles within the cells was observed by autoradiography to respond the existence of 125 I-NGF inside the cells. DNA damage was evaluated by comet assay and micronuclei forming assay. The proportion of cells in G0/G1 or S p hase was determined by flow cytometry. Results Minimal effective concentration of 125I-NGF was 592. 0 kBq/ml. Under thisconcentration, 125I-NGF could be transported to the nuclei of U251 and caused DNA damage. Being treated with 125I-NGF, U251 clone forming rate was (0. 02 ± 0. 01 ), compared to control group (0. 33 ± 0. 02),the proliferation of U251 was inhibited remarkably (P <0. 01 ). The proportion of cells in S phase ( 10. 69± 0. 02) was decreased, but that in Go/G1 phase ( 75. 10 ± 0. 22 ) increased remarkably ( P < 0. 01 ).Conclusion After being iodinated with 125I,125I-NGF can be transported to nuclei and causes DNA damage in U251. 125I-NGF has specific lethal effect on U251 cells in S phase.
Key words:
Radionuclide; Targeted therapy; Glioma
Objective To study the expression of TGF-β_1 and FⅧRAg in human acoustic neuroma and the correlation of TGF-β_1 to tumor angiogenesis.Method Expression of TGF-β_1 and FⅧRAg was detected by immunohistochemistry in 69 cases of acoustic neuroma.Then analyses of variance and linear correlation analysis were carried out.Results In solid and recurrence groups,the correlation of TGF-β_1 to microvascular density(MVD) was positive,and in cystic degenerative group,there was no correlation.Conclusions TGF-β_1 and MVD can be used as objective parameters to evaluate the biological behavior of acoustic neuroma,and can be taken as an important factor to prognosticate the tumor progression and recurrencef.
例1,兄,40岁,因左腰部不适半年,无痛性全程血尿2 d,于2004年7月入院.该患者于1996年曾因脑占位性病变而手术,术后诊断颈髓血管母细胞瘤,同时发现双侧肾囊肿,2003年11月因附睾头部肿物增大伴胀痛在我院行双侧附睾乳头状囊腺瘤切除术(在此20年前兵役体检时发现双侧附睾头部稍肿大,当时未引起重视).此次入院体检发现左肾区膨隆,可触及肿物,压痛和叩击痛.CT及B超显示肾内占位性病变,大小8.5 cm ×9.8 cm ×13.2 cm。
Objective
To investigate the effects of butylphthalide injection on cerebral blood flow (CBF) perfusion and cognitive function in patients with acute cerebral infarction accompanied by cognitive disorder.
Methods
From September 2016 to September 2017, 80 patients with acute cerebral infarction and cognitive impairment were admitted to the Department of Neurology, Yan’an Hospital of Kunming Medical University. They were assigned to an observation group (n=40) and a control group (n=40). The control group received conventional treatment while the observation group received butylphthalide injection in addition to conventional treatment. The treatment lasted for 14 days for both groups. Before and after treatment, dynamic susceptibility contrast-enhanced perfusion-weighted imaging (DSC-PWI) was used to measure the CBF parameters in the cerebral ischemic region, and Montreal Cognitive Assessment (MoCA) was used to evaluate the changes in cognitive function.
Results
After treatment, rCBF and rCBV increased significantly and rMTT and rTTP decreased significantly in the observation group (P<0.05). After treatment, there were significant improvements in MoCA subscores and total score in the observation group (P<0.05). In the observation group, the post-treatment increases in rCBV and rCBF were positively correlated with increased MoCA total score (r=0.474, P=0.013; r=0.282, P=0.027), and the post-treatment decreases in rMTT and rTTP were negatively correlated with increased MoCA total score (r=-0.294, P=0.021; r=-0.382, P=0.019).
Conclusion
Butylphthalide injection can safely improve CBF perfusion in the focal region and cognitive function in patients with acute cerebral infarction, with no obvious adverse reactions.
Key words:
Butylphthalide; Cerebral infarction; Acute stage; Cognitive dysfunction; Cerebral blood flow perfusion
Objective To explore the action mechanism of hypoxia inducible factor-1α (HIF-1α)on human osteosarcoma cells. Methods After hypoxic treatment to human osteosarcoma cell line, additional mutations were made by site-directed mutagenesis to create HIF-1α (PP) mutants. CD-1 nude mice were used for bilateral subcutaneous injections to evaluate the tumor cell tumorigenesis. Cells were seeded for 2 weeks, the total number of colonies per well was calculated and the anchorage-independent growth was analyzed. Cell proliferation was assayed by cell viability assay, and cell invasion was determined by the total number of invading cells and presented as mean ± SEM. Results The functions of the HIF-1α-ARNT pathway and the HIF-1α-c-Myc pathway were inactivated respectively by site-directed mutagenesis in the context of a stabilized HIF-1α. In accordance with diminished tumor-suppressing activities, both HIF-1α(PP) and HIF-1α (PP) + RFC cells exhibited a remarkable gain of anchorage-independent growth, and the total number of colonies per well was 1480 ± 8 and 1750 ± 6 respectively. Tumorigenicity of HIF-1α(PP) and HIF-1 α (PP) + RFC was all 100%, but US201 and HIF-1 α (PP) + VAT had no tumorigenicity. They also showed a marked increase in cell proliferation and Matrigel invasion, the cell viability of HIF1 α (PP) and HIF-1 α (PP) + VAT was 11 000 ± 3 and 10 900 ± 5, but the cell viability of HIF-1 α (PP)+ RFC and HIF-1α (PP) + RFC + VAT was only 2210 ± 6 and 1880 ± 8 respectively. Whereas inactivation of the HIF-1α-c-Myc pathway abrogated such increase, and the tumorigenicity was decreased to 20%.Gain of aggressive malignant traits required the HIF-1α-c-Myc pathway. Conclusion HIF-α-c-Myc pathway plays an essential role in mediating hypoxic effects on malignant progression via genetic alterations,resulting in formation of malignant tumors with aggressive local invasion and epithelial-mesenchymal transition.
Key words:
Hypoxia; Tumor progression; Epithelial-mesenchymal transition
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