To provide an evidence for clinical application, the distribution and radioimmunoimaging of 131I-labeled angiostatin in tumor-bearing mice were studied. Angiostatin was labeled with 131 I by the conventional chloramines T (Ch-T) method and injected into C-57 mice bearing Lewis lung cancer. The biodistribution of 131 I-angiostatin and whole body ECT imaging were studied at various intervals after injection. The average percentage of ID/g was 12. 48, 18. 56 and 23. 17 for tumor and 7. 04 ,5. 47 and 1. 73 for liver at 48, 96, 144 hours postinjection, respectively. The T/NT ratios were 1. 77, 3. 39 and 13. 39 for liver at 48 ,96 and 144 hours postinjection, respectively. The tumor was showed clearly at 96 hours after injection . The quality of tumor imaging was relevant to the T/NT ratio . The results demonstrated that the 131I-angiostatin binds specifically to the receptor on endothelial cells in the tumor and may also possess the capability of locating lung cancer tissue.

BACKGROUND: Angiostatin(AS) can effectively inhibit proliferation and migration of vascular endothelial cells and also inhibit tumor angiogenesis.OBJECTIVE: To observe the inhibitory action of angiostatin, 131I and 131 I labeled angiostatin(131I-AS) on proliferation of human umbilical vein endothelial cell ECV304 and on mass and volume of Lewis lung carcinoma (LLC) in mice.DESIGN: A randomized controlled trial with human umbilical vein endothelial cell ECV304 and Lewis lung carcinoma tumors growing in C57BL/6 mice as subjects of research.SETTING: A radiological lab and a nuclear medicine department in a military university.MATERIALS: Totally 28 LLC carrying male C57BL/6 mice, weighing(20± 2) g, 5 - 7 weeks old.METHODS: 131I-AS solutions of four concentrations were made: solution A(131I 0. 74 GBq/L, AS 0. 5 mg/L); solution B(131I 0.74 GBq/L, AS 16 mg/L); solution C(131I 1.48 GBq/L, AS 0.5 mg/L); solution D(131I 1.48 GBq/L, AS 16 mg/L). The effect of 131I-AS, AS alone and 131I alone on proliferation of human umbilical vein endothelial cell ECV304 was observed with MTT method. The 28 tumor carrying mice were randomly assigned into 4 groups, in each of which was injected 0.3 mL of 131I AS(131I 11.1 MBq and AS 2.5 mg/kg), AS(2.5 mg/kg), 131I(11.1MBq) and saline respectively for twice with 7 days interval. Then the change in tumor mass and volume was observed.MAIN OUTCOME MEASURES: ① The inhibition rate on cell proliferation with MTT method; ② Change in tumor mass and volume.RESULTS: ① The inhibition rate of AS alone(0. 5 -64 mg/L) on ECV304 was (7.3 ± 3.5) % - (41.9 ± 4. 3 )% ( P = 0. 003 vs AS of 0). The inhibition rate of the 4 concentrations of 131I-AS on ECV304 was(23.9±2.8)% ,(58.2±3.9)%, (39. 1 ±4. 1)% and(78.4 ±5.4)%, which were much higher than AS alone or 131I alone( P =0. 000 3) . ② The mean volume of LLC in the four groups were (3 943 ± 236), (5 219 ± 351 ), ( 1 963 ± 126),(7 353 ±350) mm3 respectively. Compared with saline group, the tumor inhibiton rate in the other 3 groups were 46.4% , 29.0% , 73.3% respectively( P =0. 000 1 ).CONCLUSION: 131I-AS inhibits proliferation of endothelial cells in vitro and inhibits LLC growth in vivo and it outdoes AS or 131I alone.

Objective:To study the functional connectivity (FC) and metabolic effective connectivity (MEC) patterns of the default mode network (DMN) in healthy male adults based on a novel hybrid PET/MR system.Methods:Fifteen healthy male adults with median age of 29 years were recruited locally in Xi′an from January to May 2019. All subjects went through PET/MR scan to get the whole brain 18F-fluorodeoxyglucose (FDG) PET, resting-state functional MRI (fMRI) and magnetization prepared rapid gradient echo (MPRAGE) T 1 weighted imaging data. CONN18b and statistical parametric mapping (SPM) 12 softwares were used to analyze data. The voxel-wise FC and FDG metabolic data were extracted within 4 sub-networks of DMN, which included medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC) and bilateral lateral parietal (LP). The FC and MEC between 4 sub-networks were calculated based on merged resting-state fMRI and metabolic data, and analyzed by one-sample t test separately, with Bonferroni correction. Results:FC pathways were all significant within 4 sub-networks of DMN ( t values: 6.00-7.71, all P<0.008, Bonferroni corrected). Meanwhile, there were significant bi-directional MEC between MPFC and PCC(MPFC to PCC: t=10.03; PCC to MPFC: t=3.73, both P<0.004, Bonferroni corrected), as well as between bilateral LP (LP_L to LP_R: t=5.28; LP_R to LP_L: t=4.76, both P<0.004, Bonferroni corrected). There were significant uni-directional MEC from both MPFC and PCC to bilateral LP ( t values: 3.44-6.93, all P<0.004, Bonferroni corrected). Conclusions:Special FC and MEC patterns exist within DMN. The closely interrelated MPFC and PCC play more important roles in DMN, and they may mediate LP jointly. The novel integrated PET/MR system will bring new perspective on the organization of brain networks, which may deepen the comprehensive understanding of DMN.

Objective:To investigate the changes in total radioactivity in patient body with differentiated thyroid carcinoma (DTC) after 131I treatment and the factors influencing its metabolism. Methods:The clinical data from 218 patients after DTC treatment in the Department of Nuclear Medicine, the Second Affiliated Hospital of Air Force Medical University from September 2021 to April 2022 were retrospectively analyzed. Based on administrated 131I dose, 171 patients were divided into low-dose group (≤ 3.7 GBq) and 47 into high-dose group (>3.7 GBq) . A whole body dynamic radiation monitoring system was used to measure the in vivo residual activity of 131I 24, 48 and 72 h after 131I administration and to explore their influencing factors. Results:24, 48 and 72 h after adimination of 131I, the residual activity of 131I in the low-dose group patients was significantly lower than in the high-dose group patients ( t= -7.46, -3.31, -2.01, P<0.05) . The discharge compliance rate at 24 and 48 h in the low-dose group was significantly higher than that in the high-dose group (21.0% vs. 4.3%, 98.2% vs. 89.4%, χ2 = 7.23, 5.91, P<0.05) , and all patients could meet the discharge criteria at 72 h. Univariate analysis showed that the residual 131I activity at 24 and 48 h was dependent on age, body mass index (BMI) , basal metabolism rate (BMR) and thyroid stimulating hormone (TSH) . As have been shown by multiple linear regression analysis, in the low-dose group, the older age, the higher BMR and the higher TSH level at 24 h tended to the higher 131I residual activity in the body. At 48 h, the higher BMI and the higher TSH level lead to the higher 131I residual activity in patient body. Meanwhile, in the high-dose group, the higher age and BMR at 24 h, tended to the higher in vivo131I residual activity. The influencing factors were analyzed in terms that 131I residual activity reaching 400 MBq in patient body at 24 and 36 h. The result showed that at 24 h the lower TSH level leaded to the lower 131I residual activity in patient body. At 36 h, the younger age, the lower TSH level, and the smaller 131I treatment dose tended to the lower in vivo131I residual activity. Conclusions:Age, BMI, BMR and TSH levels are the influencing factors for the change in total activity in patient body after 131I treatment of DTC. Radiation dose assessment based on the above indicators can provide a reference for adjusting the length of hospitalization time.

BACKGROUND:Croton cream can activate ERK pathways and have anti-apoptotic effects on neuronal cells.It is not clear whether it synergistically exerts anti-apoptotic effects by inhibiting the activation of JNK and p38 pathways. OBJECTIVE:To explore the effects and mechanisms of croton cream on neuronal damage and apoptosis in the ischemic cortex of rats with cerebral ischemia-reperfusion injury. METHODS:(1)Ninety Sprague-Dawley rats were randomly divided into sham operation group,model group,croton cream low-dose group,croton cream medium-dose group,croton cream high-dose group and nimodipine group,with 15 rats in each group.Except for the sham operation group,animal models of middle cerebral artery occlusion were prepared in rats by the thread method.Rats in the three croton cream groups were given 20,40,and 60 mg/kg croton cream,respectively.Rats in the sham operation and model groups were given the same amount of normal saline,once a day,for 7 consecutive days.The optimal concentration of croton cream,namely the high dose of croton cream,was selected based on neurological deficit score,TTC staining,brain tissue water content,hematoxylin-eosin staining and Nissl staining.(2)Another 120 Sprague-Dawley rats were randomly divided into sham operation group,model group,croton cream group,JNK inhibitor group,croton cream+JNK inhibitor group,p38 MAPK inhibitor group,croton cream+p38 MAPK inhibitor group,and nimodipine group,with 15 rats in each group.Animal models of middle cerebral artery occlusion were prepared using the thread method in all the groups except in the sham operation group.Thirty minutes before modeling,10 μL of SP600125(JNK inhibitor)and 10 μL of SB203580(p38 MAPK inhibitor)were injected into the lateral ventricle of the rats,respectively.Rats in croton cream groups were intragastrically given 60 mg/kg croton cream.Seven days later,the JNK/p38 MAPK signaling pathway,apoptosis-related proteins and cell apoptosis were detected by western blot,TUNEL staining and flow cytometry,respectively. RESULTS AND CONCLUSION:(1)Compared with the sham operation group,neurological deficit score,cerebral water content,cerebral infarction volume and apoptosis rate were significantly increased in the model group(P<0.05),where nerve cells showed scattered distribution.Compared with the model group,neurological deficit score,water content of brain tissue and cerebral infarction volume were significantly decreased in the croton cream medium-dose group,high-dose group and nimodipine group(P<0.05),and the pathological morphology of nerve cells was significantly improved.(2)Compared with the JNK inhibitor group,p-JNK/JNK,p-p38/p38 and Bax expressions in rat brain tissue and the apoptotic rate were significantly decreased in the croton cream+inhibitor groups(P<0.05),while the expression of and Bcl-2 was significantly increased(P<0.05).To conclude,croton cream may inhibit the activation of JNK/p38 MAPK signaling pathway and reduce neuronal apoptosis to achieve neuroprotective effects in rats with cerebral ischemia-reperfusion injury.

Objective: To explore and optimize the primary culture method of neonatal mouse hippocampal neurons in vitro．To construct a G-protein-coupled receptor kinase 2 ( GRK2) knockout HT22 cell line． Methods : Hippocampal tissue of C57BL6 /J mice on day 1－2 was taken，digested with trypsin and pipetted to form a cell suspension，and supplement was added to Neurobasal-A medium to maintain cell growth． CRSIPR / Cas9 gene editing technique was used to construct HT22-GRK2 －/ － cell line，and the knockout efficiency of GRK2 was detected by immunofluorescence staining and Western blot. Results : Primary hippocampal neurons of newborn mice were put into six-well plates with 3 × 107 /well using a serum-free culture method，which could get a high purity and good activity ; HT22-GRK2 －/ － cell line was constructed successfully． Conclusion The primary culture method of mouse hippocampal neurons was successfully established and optimized，and HT22-GRK2 －/ － cell line was successfully constructed by CRSIPR / Cas9 gene editing technique.