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Objective:To fulfill the automatic radiolabeling of the norepinephrine transporter (NET) trancer 18F-meta-fluorobenzylguanidine (mFBG), and explore the 18F-mFBG PET/CT imaging effect of pheochromocytoma. Methods:On the basis of the chemical structure of mFBG, a spirocyclic iodonium ylide was used as the precursor to undergo a 3-step reaction sequence (radiofluorination, deprotection and neutralization) on AllinOne synthesis module. Purification by high performance liquid chromatography and formulation were conducted to generate 18F-mFBG. The corresponding quality control tests of 18F-mFBG product was performed. Afterwards, a postoperative patient with pheochromocytoma underwent 18F-mFBG PET/CT imaging. Results:The radiosynthesis was accomplished within 70 min, and 18F-mFBG was obtained in (17.8±2.4)% non-decay-corrected radiochemical yield ( n=5), with radiochemical purity >97% and molar activity >59.2 GBq/μmol. Sterility test, bacterial endotoxins test, abnormal toxicity test and the acetonitrile residue all met the requirements of Pharmacopoeia of the People′ s Republic of China (2020 Volume Ⅳ). The 18F-mFBG PET/CT imaging disclosed high uptake in pheochromocytoma and clear localization of lesions. Conclusions:The automatic radiolabeling of the NET targeted tracer 18F-mFBG is successfully realized by commercially available synthesis module, and the production quality meets all requirements for clinical translation. 18F-mFBG has a potential to image neuroendocrine lesions in clinical setting.
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Objective To investigate the effects and regulating mechanisms of matrix metalloproteinase 9 (MMP-9) gene silencing on aquaporin 4(AQP4) expression in astrocytes induced by oxygen-glucose deprivation.Methods Cerebral cortical astrocytes from 2 days newborn SD rats were undergone the primary culture.The ischemic cell model was established by oxygen-glucose deprivation.This experiment were divided into control group,negative control group and MMP-9 gene silencing group.The leakage rate of lactated dehydrogenase (LDH)was detected by chromatoptometry.The MMP-9 gene silencing was carried out by Lentivirus transfection.Real-time fluorescence quantitative PCR and Western blot were used to detect the expression levels of AQP4 and MMP-9.The expressions of PKA,PKC,PKG and CaMK Ⅱ were determined by Western blot.Results Compared with control group,LDH leakage rate was significantly higher in astrocytes induced by oxygen-glucose deprivation(t=13.35,P＜0.01).The expression of MMP-9 mRNA in astrocytes in MMP-9 gene silencing group(0.412±0.297) decreased significantly compared with that in negative control group(1.118 ± 0.240) (t =-4.964,P＜ 0.05).The expression of AQP4 mRNA in astrocytes in MMP-9 gene silencing group(1.002±0.082) decreased significantly compared with that in negative control group(1.442±0.066) (t=-9.886,P＜0.01).The expression of AQP4 protein in astrocytes in MMP-9 gene silencing group(0.643±0.036)decreased significantly compared with that in negative control group(1.000± 0.069)(t=-11.073,P＜0.01).The expression of PKC protein in astrocytes in MMP-9 gene silencing group (0.198±0.110)decreased significantly compared with that in negative control group (0.980± 0.232) (t =-7.218,P＜0.01).The expressions of PKA(t=0.875),PKG(t=0.818) and CaMK Ⅱ (t=0.933) protein had no statistically significant difference between negative control group and MMP-9 gene silencing group(all P＞0.05).Conclusion The permeability of astrocytes is increased by oxygen-glucose deprivation.Gene silencing MMP-9 could induce expression of AQP4 mRNA and protein decreased,and MMP-9 may regulate AQP4 expression by regulating PKC activity.
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Objective To explore the risk factors of poststroke infection after cerebral infarction. Methods We consecutively included 283 patients with acute ischemic infarcts confirmed by diffusion-weighted imaging (DWI) within 72 hours from Guangxi stroke center. Based on infection status, patients were divided into Not infection group(n=198) and infection group (n=85). The serum cortisol and plasma IL-4 were assessed using chemiluminescent system and double antibody sandwich enzyme linked immunosorbent assay at admission and seventh day later,respectively. Results Compare to no infection group, smoking, mechanical ventilation, diabetes mellitus, dysphagia, COPD,level of consciousness, cortisol and IL-4 at admission, NIHSS, middle area and large area infarction, large atherosclerosis and cardiogenic infarction, left side,both side and subtentorial infarction are more liable to infection(P<0.05);After a Single-factor and Multivariate analysis,we found that cortisol(OR 3.26)and IL-4(OR 2.83)at admission,large area infarction(OR 2.67),left side(OR 3.78)and subtentorial infarction(OR 3.12)were significant correlated with infection, suggesting that they might be the independent risk factors for infection after cerebral infarction. Conclusion Immunological factors and different regional cerebral infarction may increase susceptibility to infection after stroke.
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Objective To explore the effect of apolipoprotein E deficiency on astrocyte destruction in the ex vivo spinal cord slice model. Methods Vibratome-cut transverse spinal cord slices from C57BL/6 postnatal day 7 ApoE -/-mice and wild-type mice were cultured on transwell porous supports. After 7 days in the culture , spinal cord slices were exposed to LPS for 5 days. The expression of AQP4, GFAP and Iba1 was detected by immunofluorescence. The concentration of TNF-α and NO were detected by ELISA and method of nitrate reductase, respectively. Results Marked loss of AQP4 and GFAP staining were shown in LPS-affected groups, not in the control group, and the lesion score was higher in ApoE-/-group than WT-group (P<0.05). In addition, the expression of Iba1 and concentration of TNF-α, NO in the LPS-affected groups were more than that of the control group (P < 0.05), and they were higher in the ApoE-/-LPS group than the WT-LPS group (P < 0.05). Conclusions ApoE deficiency exacerbates astrocyte injury, likely through promoting the release of pro-inflammatory mediators from microglia.
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BACKGROUND: Precise clinical treatment of talar ischemic necrosis remains controversial at present.OBJECTIVE: To observe the changes in the stress and its distribution on talar trochlear articular surface in case of talar necrosis at different levels.METHODS: The present study adopted eight ankle specimens to establish the three-dimensional finite element model of ankle. Through changes in the talar necrosis volume of these models, this study analyzed the change law of talar trochlear articular surface stress and its distribution and calculated the critical necrosis volume of traumatic foot and ankle arthritis or talar collapse that may be induced by talar ischemic necrosis.RESULTS AND CONCLUSION: The experiment successfully established the three-dimensional finite element model of ankle. This study found that talar trochlear articular surface stress distribution showed little change in case of talar medial and lateral necrosis at a lower level; when medial talar necrosis volume reached (26.6±1.5)%, and lateral talar necrosis volume reached (35.0±2.5)%. Stress concentration phenomenon occurred in the boundary area between talar necrosis tissue and normal osseous tissue, and the stress area took the shape of irregular pattern. It is suggested that surgical treatment should be considered due to the high-risk induction of ankle-foot traumatic arthritis or talar collapse.