OBJECTIVE: To optimize the extraction technology of ardicrenin from Ardisia crenata.METHODS: The content of ardicrenin was determined by RP-HPLC. The extraction technology was optimized by orthogonal experiment with the extraction rate of ardicrenin as evaluation index and with the volume fraction of ethanol,the extraction temperature,extraction time and extraction times as factors.RESULTS: The optimum extraction technology was determined as follows: 80%ethanol was used as solvent;the extraction temperature was 80 ℃;the extraction time was 20 min and the extraction was conducted for 3 times.The extraction rate of ardicrenin was 6.04%.CONCLUSION: The optimized extraction technology is feasible and reproducible,and it provides theoretical basis for mass extraction of the ardicrenin from A.crenata.

Objective: To investigate the association between ABCC2 gene polymorphisms and cyclosporine-induced liver injury in re-nal transplant recipients. Methods: The renal transplant recipients were divided into the liver injury group and the control group. Five single nucleotide polymorphisms ( rs4919395, rs2804398, rs4148394, rs4148397 and rs3740065) of ABCC2 were detected by high-throughput technique. The genotypes and haplotypes were analyzed between the groups. Results: There were 35 patients and 182 patients respectively in the liver injury group and the control group. No significant differences in alleles and genotypes were found between the groups (P>0. 05), and the SNP haplotypes showed no significant difference between the groups (P>0. 05). Conclusion: There is no association of ABCC2 polymorphisms (rs4919395, rs2804398, rs4148394, rs4148397 and rs3740065) with the liver injury induced by cy-closporine.

Objective To explore the correlation between changes of gray matter volume and related cognitive impairment domains in patients with cognitive impairment of cerebral small vessel disease(CSVD)based on 7.0T magnetic resonance imaging(MRI)and voxel-based morphometry(VBM).Methods All subjects were recruited from the study on Correlation between Cerebral Deep Medullary Vein Morphology and Cognitive Impairment due to Cerebral Small Vessel Disease(registration No.:ChiCTR2100045136)from September 2021 to June 2023.We retrospectively enrolled CSVD patients with cognitive impairment as CSVD group and healthy controls with matched age,gender and education level as control group according to inclusion and exclusion criteria.Montreal cognitive assessment(MoCA)scale(Beijing version)score＜26 was divided into cognitive impairment.All subjects was assessed with MoCA,digit span test(DST),digit symbol substitution test(DSST),trail making test-A(TMT-A),verbal fluency test(VFT),Boston naming test(BNT)and auditory verbal learning test(AVLT).All subjects underwent 7.0T brain MRI scan to acquire T1-weighted three-dimensional magnetization prepared 2 rapid gradient echo(T1WI-MP2RAGE)for VBM analysis.General data and above cognitive function scores were compared between 2 groups.VBM analysis was used to compare the gray matter volume(GMV)between 2 groups and get mean GMV of significant brain regions of CSVD to explore the correlation between regions and cognitive function scores.Results(1)There were 18 individuals in control group,aged 55-70 years,and 19 individuals in CSVD group,aged 57-75 years.There was no significant difference in age,gender,education,body mass index,history of coronary heart disease,history of hyperlipidemia,smoking,drinking,total cholesterol,triglyceride,low density lipoprotein and high density lipoprotein between the two groups(all P＞0.05).But the proportion of hypertension and diabetes history in the CSVD group was higher than control group,and there were significant differences between the two groups(12/19 vs.5/18,7/19 vs.0;all P＜0.05).(2)The scores of MoCA scale(22.0[20.0,23.0]vs.27.0[26.0,28.0],Z=-5.242),DSST(18±9 vs.40±4,t=5.212),DST(10.6±2.5 vs.13.9±2.0,t=4.364),VFT(38±11 vs.47±8,t=3.224),AVLT-immediate memory(13±3 vs.21±4,t=6.877),AVLT-short delay recall(3.4±2.5 vs.6.9±2.2,t=4.555)and BNT(22.7±3.6 vs.27.0±2.1,t=4.357)in CSVD group were lower than those in the control group.The time taken to complete TMT-A in CSVD group was longer than the control group(93.00[76.04,125.69]s vs.29.77[25.75,40.97]s,Z=-4.832).The difference of the above between two group was statistically significant(all P＜0.01).(3)Brain parenchymal fraction in CSVD group was lower than control group,and there was significant difference between two group([78.2±4.3]％vs.[80.9±3.7]％,t=2.079,P＜0.05).VBM analysis showed that gray matter volume of right inferior temporal gyrus(rITG)and right Crus 2 of cerebellar hemisphere(rCERCRU2)in CSVD group was significantly lower than control group(both P＜0.05 and corrected by false discovery rate).(4)Partial correlation analysis showed a positive correlation between gray matter volume in rITG and AVLT-short delay recall score(r=0.543,P=0.036).Conclusions CSVD patients with cognitive impairment had gray matter atrophy in rITG and rCERCRU2 and the gray matter volume in rITG was correlated with delayed memory impairment.The results of this study need to be further verified.

ObjectiveTo conduct a visualized analysis of the research related to the use of brain-computer interface technology for stroke rehabilitation in the past ten years, and identify and predict the hot spots and hot trends in order to promote the further development of this field. MethodsThe Web of Science Core Collection database was searched for literature related to brain-computer interface technology for stroke rehabilitation from January, 2011 to October, 2022. CiteSpace 5.8.R3 was used to analyze the number of publications, countries, institutions, authors, keywords, co-citations, and grant support. Results and ConclusionA total of 592 papers were included, and the annual number of publications in this field of research showed a rapid growth trend, and the research enthusiasm continued to increase. The United States was in the leading position in this field, with the highest number of cooperative publications and the highest intermediary centrality; China had certain advantages in this field, but still needed to strengthen the exchange and cooperation with other countries/regions. Foreign institutions and authors had formed a network of close cooperative relationships, and formed a high-impact team represented by Niels Birbaumer, Cuntai Guan, Kai Keng Ang, etc.; there were poor cooperative relationships among domestic authors and institutions, and there were geographical restrictions and lack of high-impact academic groups. The keywords "motor imagery" and "recovery" formed ten major clusters and 15 prominent words with high variation rates, showing a trend of diversification in research directions. The study of the efficacy of upper limb motor rehabilitation and central mechanisms has been the hot topics in this field and will continue for some time in the future; the use of lower limb brain-computer interface systems for improving foot drop, gait and balance in stroke patients and the application of multimodal brain-computer interfaces will probably become a hot topic in the future. Finally, the use of brain-computer interface-guided neurofeedback training for cognitive and language rehabilitation in stroke also needs attention.

Pulmonary hypertension (PH) is an extremely malignant pulmonary vascular disease of unknown etiology. ADAR1 is an RNA editing enzyme that converts adenosine in RNA to inosine, thereby affecting RNA expression. However, the role of ADAR1 in PH development remains unclear. In the present study, we investigated the biological role and molecular mechanism of ADAR1 in PH pulmonary vascular remodeling. Overexpression of ADAR1 aggravated PH progression and promoted the proliferation of pulmonary artery smooth muscle cells (PASMCs). Conversely, inhibition of ADAR1 produced opposite effects. High-throughput whole transcriptome sequencing showed that ADAR1 was an important regulator of circRNAs in PH. CircCDK17 level was significantly lowered in the serum of PH patients. The effects of ADAR1 on cell cycle progression and proliferation were mediated by circCDK17. ADAR1 affects the stability of circCDK17 by mediating A-to-I modification at the A5 and A293 sites of circCDK17 to prevent it from m1A modification. We demonstrate for the first time that ADAR1 contributes to the PH development, at least partially, through m1A modification of circCDK17 and the subsequent PASMCs proliferation. Our study provides a novel therapeutic strategy for treatment of PH and the evidence for circCDK17 as a potential novel marker for the diagnosis of this disease.