Objective To explore the international research hotspots and trends in remote ischemic conditioning(RIC).Methods The literature on RIC research from January 1,2000 to December 12,2024 in the core collection of Web of Science database were retrieved.Microsoft Excel,CiteSpace and VOSviewer were used for bibliometric and visual analysis of the retrieved literature,including the number of literature published per year,countries,institutions,journals,authors,cited references,keywords and burst keywords.Results(1)The relevant literature on RIC from January 1,2000 to December 12,2024 was published in 456 journals by 6 688 authors from 1 597 institutions in 59 countries,and 32 064 citations from 3 860 journals were cited.The number of RIC relevant literature published in the past decade was high,and the number of literature published in 2017 was the highest,with 145 papers.(2)The country with the largest number of publications was China(448 papers),followed by the United States(240 papers).The institution with the largest number of publications was Capital Medical University of China(103 papers),followed by Aarhus University in Denmark(63 papers).The top three journals that published relevant literature were Plos One(37 papers),Basic Research in Cardiology(32 papers)and Journal of Surgical Research(26 papers).The top three authors who published relevant literature were Ji Xunming(60 papers),Heusch G(30 papers)and Ren Changhong(29 papers).(3)The most cited article among cited references was Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium(414 times).The total number of co-citation journals was 3 860 and the most frequent co-citation journal was Circulation(3 933 times).(4)A total of 4 089 keywords were extracted,and the top three keywords were"reperfusion injury""remote ischemic preconditioning"and"cardioprotection".The top three strength of burst keywords were"remote ischemic conditioning""ischemic stroke"and"thrombolysis".In the past five years,the burst keywords with high strength were"thrombolysis""international clinical recommendations""safety""ischemic stroke""recovery"and"efficacy".Conclusions In the past decade,RIC related literature has maintained a high number of publications.There is close cooperation among countries,institutions and scholars.Capital Medical University of China plays an important role in international RIC related research.RIC related research mainly focuses on the mechanism of ischemia-reperfusion protection,cardioprotection and ischemic stroke.The clinical application,efficacy and safety of RIC in ischemic stroke have become trends and hotspots in international RIC researches.

BACKGROUND:Relatively or absolutely active bone resorption function of osteoclasts is one of the causative factors of osteoporosis. Therefore,how to inhibit the formation of osteoclasts and reduce the bone resorption activity is a key element in the prevention and treatment of osteoporosis. Liquiritin,which is derived from licorice,plays a role in the clinical treatment of bone diseases,but there are fewer studies addressing the application of liquiritin in osteoporosis and the mechanism is unknown.OBJECTIVE:To confirm,through both in vivo and in vitro experiments,that liquiritin inhibits osteoclast differentiation and alleviates bone loss.METHODS:Cell counting kit-8 was used to detect whether Liquiritin exerts toxic or proliferative effects on mouse bone marrow-derived macrophages,and tartrate-resistant acid phosphatase staining was performed to observe the effect of liquiritin in inhibiting osteoclast differentiation. The affinity of liquiritin binding to proteins related to osteoclast differentiation was verified by network pharmacology. RT-PCR and western blot assays were performed to detect the inhibitory effects of liquiritin on osteoclast-specific protein and gene expression as well as relevant signaling pathways. Finally,the mitigating effect of liquiritin on bone loss was verified in the C57BL/6J mouse osteoporosis model.RESULTS AND CONCLUSION:Liquiritin,at concentrations of 20 μmol/L and below,could inhibit the formation and differentiation of osteoclasts. Concurrently,it exhibited a high affinity with osteoclast-specific proteins such as nuclear factor of activated T-cells 1,Cathepsin K,c-Fos,and matrix metalloproteinase 9,and reduced the relative expression levels of these genes and proteins. Liquiritin could also effectively lower the phosphorylation expression level of JNK in the MAPK signaling pathway at the 15th,30th,45th,and 60th minutes,and it could salvage the degradation of nuclear factor-κB inhibitor α in the nuclear factor-κB signaling pathway at the 60th minute. In vivo experiments demonstrated that liquiritin could mitigate bone loss caused by osteoclasts and improve parameters related to trabecular bone. To conclude,liquiritin possesses the capacity to inhibit osteoclast differentiation and alleviate bone loss,thereby exerting a protective role against osteoporosis.

Objective:To investigate the effect of deubiquitinating enzymes(DUBs) USP2 on depressive-like behavior and hippocampal NF-κB expression in mice.Methods:(1) USP2 silencing experiment: Two USP2 silencing interference sequences with the highest knockdown efficiency were screened and cloned into a lentivirus vector. Mice were microinjected with lentivirus vector into both sides of hippocampus to silence the USP2 gene, and depressive behavior and USP2 protein expression in hippocampal tissue were observed. (2) Venlafaxine intervention experiment: total 32 healthy male C57BL/6 mice were randomly divided into virus control group, Venlafaxine group, USP2 silencing group, and USP2 silencing+ Venlafaxine group according to the random number table method, with 8 mice in each group. Mice were injected with lentivirus into both side of the hippocampus, and 7 days later, they were given intraperitoneal injection of Venlafaxine (5 mg/kg, once a day, for a total of 14 days). After the administration, the depressive behavior of mice was detected by forced swimming test(FST) and tail suspension test(TST), and the expression levels of USP2, p-IκBα, IκBα, p-NF-κB p65, and NF-κB p65 in the hippocampus of mice were detected by Western blot.SPSS 25.0 and GraphPad Prism 8.0 were used for data processing and chart drawing.The t-test was used for comparison between two groups, One-way ANOVA was used for comparison among multiple groups, and Tukey HSD or LSD- t was used for post hoc pairwise comparison when there was homogeneity of variance. Results:(1)The results of the USP2 silencing experiment showed that both screened USP2 silencing sequences had good gene knockout effects. The expression levels of USP2 protein in the hippocampus of mice injected with USP2 silencing virus were lower than those of the negative control virus groups (both P<0.05). The immobility time of mice in the FST and TST was higher than that of the negative control virus group (both P<0.05). (2)Venlafaxine intervention experiment: There were statistically significant differences in immobility time among the four groups of mice in the FST and TST ( F=8.90, 4.41, both P<0.05). The immobility time of FST and the immobility time of TST in the USP2 silencing+ Venlafaxine group ((48.13±12.76) s, (77.38±12.35) s) were lower than those in the USP2 silencing group((129.88±11.67)s, (148.29±15.31)s) (both P<0.05). There were statistically significant differences in the expression levels of USP2, p-IκBα, and p-NF-κB p65 proteins in the hippocampal tissues of the four groups of mice ( F=8.39, 5.78, 21.32, all P<0.05).The expression level of USP2 protein in the USP2 silencing group(0.49±0.07) was lower than that in the USP2 silencing+ Venlafaxine group(0.79±0.08) and virus control group(1.00±0.07)(both P<0.05), while the expression levels of p-IκBα, p-NF-κB p65 protein (1.63±0.18, 2.14±0.24) were higher than those in the virus control group (1.00±0.06, 1.00±0.04) and the USP2 silencing+ Venlafaxine group (0.70±0.23, 0.68±0.09) (both P<0.05). Conclusion:USP2 scilencing can induce depressive-like behaviors in mice. Venlafaxine ameliorates USP2 silencing-induced depressive-like behaviors, which may be associated with the hippocampal NF-κB signaling pathway.

Objective:To investigate the effect of deubiquitinating enzymes(DUBs) USP2 on depressive-like behavior and hippocampal NF-κB expression in mice.Methods:(1) USP2 silencing experiment: Two USP2 silencing interference sequences with the highest knockdown efficiency were screened and cloned into a lentivirus vector. Mice were microinjected with lentivirus vector into both sides of hippocampus to silence the USP2 gene, and depressive behavior and USP2 protein expression in hippocampal tissue were observed. (2) Venlafaxine intervention experiment: total 32 healthy male C57BL/6 mice were randomly divided into virus control group, Venlafaxine group, USP2 silencing group, and USP2 silencing+ Venlafaxine group according to the random number table method, with 8 mice in each group. Mice were injected with lentivirus into both side of the hippocampus, and 7 days later, they were given intraperitoneal injection of Venlafaxine (5 mg/kg, once a day, for a total of 14 days). After the administration, the depressive behavior of mice was detected by forced swimming test(FST) and tail suspension test(TST), and the expression levels of USP2, p-IκBα, IκBα, p-NF-κB p65, and NF-κB p65 in the hippocampus of mice were detected by Western blot.SPSS 25.0 and GraphPad Prism 8.0 were used for data processing and chart drawing.The t-test was used for comparison between two groups, One-way ANOVA was used for comparison among multiple groups, and Tukey HSD or LSD- t was used for post hoc pairwise comparison when there was homogeneity of variance. Results:(1)The results of the USP2 silencing experiment showed that both screened USP2 silencing sequences had good gene knockout effects. The expression levels of USP2 protein in the hippocampus of mice injected with USP2 silencing virus were lower than those of the negative control virus groups (both P<0.05). The immobility time of mice in the FST and TST was higher than that of the negative control virus group (both P<0.05). (2)Venlafaxine intervention experiment: There were statistically significant differences in immobility time among the four groups of mice in the FST and TST ( F=8.90, 4.41, both P<0.05). The immobility time of FST and the immobility time of TST in the USP2 silencing+ Venlafaxine group ((48.13±12.76) s, (77.38±12.35) s) were lower than those in the USP2 silencing group((129.88±11.67)s, (148.29±15.31)s) (both P<0.05). There were statistically significant differences in the expression levels of USP2, p-IκBα, and p-NF-κB p65 proteins in the hippocampal tissues of the four groups of mice ( F=8.39, 5.78, 21.32, all P<0.05).The expression level of USP2 protein in the USP2 silencing group(0.49±0.07) was lower than that in the USP2 silencing+ Venlafaxine group(0.79±0.08) and virus control group(1.00±0.07)(both P<0.05), while the expression levels of p-IκBα, p-NF-κB p65 protein (1.63±0.18, 2.14±0.24) were higher than those in the virus control group (1.00±0.06, 1.00±0.04) and the USP2 silencing+ Venlafaxine group (0.70±0.23, 0.68±0.09) (both P<0.05). Conclusion:USP2 scilencing can induce depressive-like behaviors in mice. Venlafaxine ameliorates USP2 silencing-induced depressive-like behaviors, which may be associated with the hippocampal NF-κB signaling pathway.

Objective To explore the international research hotspots and trends in remote ischemic conditioning(RIC).Methods The literature on RIC research from January 1,2000 to December 12,2024 in the core collection of Web of Science database were retrieved.Microsoft Excel,CiteSpace and VOSviewer were used for bibliometric and visual analysis of the retrieved literature,including the number of literature published per year,countries,institutions,journals,authors,cited references,keywords and burst keywords.Results(1)The relevant literature on RIC from January 1,2000 to December 12,2024 was published in 456 journals by 6 688 authors from 1 597 institutions in 59 countries,and 32 064 citations from 3 860 journals were cited.The number of RIC relevant literature published in the past decade was high,and the number of literature published in 2017 was the highest,with 145 papers.(2)The country with the largest number of publications was China(448 papers),followed by the United States(240 papers).The institution with the largest number of publications was Capital Medical University of China(103 papers),followed by Aarhus University in Denmark(63 papers).The top three journals that published relevant literature were Plos One(37 papers),Basic Research in Cardiology(32 papers)and Journal of Surgical Research(26 papers).The top three authors who published relevant literature were Ji Xunming(60 papers),Heusch G(30 papers)and Ren Changhong(29 papers).(3)The most cited article among cited references was Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium(414 times).The total number of co-citation journals was 3 860 and the most frequent co-citation journal was Circulation(3 933 times).(4)A total of 4 089 keywords were extracted,and the top three keywords were"reperfusion injury""remote ischemic preconditioning"and"cardioprotection".The top three strength of burst keywords were"remote ischemic conditioning""ischemic stroke"and"thrombolysis".In the past five years,the burst keywords with high strength were"thrombolysis""international clinical recommendations""safety""ischemic stroke""recovery"and"efficacy".Conclusions In the past decade,RIC related literature has maintained a high number of publications.There is close cooperation among countries,institutions and scholars.Capital Medical University of China plays an important role in international RIC related research.RIC related research mainly focuses on the mechanism of ischemia-reperfusion protection,cardioprotection and ischemic stroke.The clinical application,efficacy and safety of RIC in ischemic stroke have become trends and hotspots in international RIC researches.

BACKGROUND:Relatively or absolutely active bone resorption function of osteoclasts is one of the causative factors of osteoporosis. Therefore,how to inhibit the formation of osteoclasts and reduce the bone resorption activity is a key element in the prevention and treatment of osteoporosis. Liquiritin,which is derived from licorice,plays a role in the clinical treatment of bone diseases,but there are fewer studies addressing the application of liquiritin in osteoporosis and the mechanism is unknown.OBJECTIVE:To confirm,through both in vivo and in vitro experiments,that liquiritin inhibits osteoclast differentiation and alleviates bone loss.METHODS:Cell counting kit-8 was used to detect whether Liquiritin exerts toxic or proliferative effects on mouse bone marrow-derived macrophages,and tartrate-resistant acid phosphatase staining was performed to observe the effect of liquiritin in inhibiting osteoclast differentiation. The affinity of liquiritin binding to proteins related to osteoclast differentiation was verified by network pharmacology. RT-PCR and western blot assays were performed to detect the inhibitory effects of liquiritin on osteoclast-specific protein and gene expression as well as relevant signaling pathways. Finally,the mitigating effect of liquiritin on bone loss was verified in the C57BL/6J mouse osteoporosis model.RESULTS AND CONCLUSION:Liquiritin,at concentrations of 20 μmol/L and below,could inhibit the formation and differentiation of osteoclasts. Concurrently,it exhibited a high affinity with osteoclast-specific proteins such as nuclear factor of activated T-cells 1,Cathepsin K,c-Fos,and matrix metalloproteinase 9,and reduced the relative expression levels of these genes and proteins. Liquiritin could also effectively lower the phosphorylation expression level of JNK in the MAPK signaling pathway at the 15th,30th,45th,and 60th minutes,and it could salvage the degradation of nuclear factor-κB inhibitor α in the nuclear factor-κB signaling pathway at the 60th minute. In vivo experiments demonstrated that liquiritin could mitigate bone loss caused by osteoclasts and improve parameters related to trabecular bone. To conclude,liquiritin possesses the capacity to inhibit osteoclast differentiation and alleviate bone loss,thereby exerting a protective role against osteoporosis.

Objective To analyze the clinical data and head imaging features of perioperative acute ischemic stroke(POAIS)with non-small cell lung cancer(NSCLC)and to explore the possible risk factors and pathogeneses of it,and to provide evidence for the prevention and treatment of POAIS.Methods Data of patients with primary NSCLC who underwent lung resection and had POAIS was retrospectively collected,and the clinical data of patients with cerebral infarction of large artery atherosclerosis(LAA)and stroke of undetermined etiology(SUE)was compared.Results There were 25 NSCLC patients with POAIS,some of whom had no history of cardiovascular and cerebrovascular diseases,and the proportion was higher in SUE.The most common excision site was left upper lobe,especially in SUE.The pathological stage and type were mainly early stage and adenocarcinoma.Most patients developed POAIS within 7 days after surgery,and mainly mild to moderate.Middle cerebral artery was the main responsible vessel and most patients'cerebral infarction locations≥3.SUE was the most common type of Trial of Org 10172 in Acute Stroke Treatment(TOAST),followed by LAA type.Compared with SUE,more patients had a history of type 2 diabetes(P=0.006)and higher preoperative fasting glucose level(P=0.013)with LAA type.Conclusion Attention should be paid to the prevention of LAA type cerebral infarction in NSCLC patients with type 2 diabetes or preoperative high fasting glucose level,and antithrombotic regimen is selected according to different etiological mechanisms of POAIS.The formation of pulmonary vein thrombosis after lung resection should be prevented and paid attention to.

Robotic-assisted percutaneous coronary intervention (R-PCI) is an innovative way of performing percutaneous coronary intervention (PCI) whereby the operator can manipulate coronary intraluminal guidewires and catheter devices by using remotely controlled technology. Performing tele-R-PCI from a remote location via fifth generation network communication technology has never been reported in China; however, if this were possible, the technique could be used to treat many patients with coronary artery disease who would otherwise not have the opportunity of treatment. The case of a 73-year-old male patient with coronary artery disease who underwent successful tele-R-PCI at 800 km from the operators is presented. Performing long-distance tele-R-PCI in patients with coronary artery disease is feasible with predictably successful outcomes when reliable network connectivity and local cardiac catheterization facilities are present.

Robotic-assisted percutaneous coronary intervention (R-PCI) is an innovative way of performing percutaneous coronary intervention (PCI) whereby the operator can manipulate coronary intraluminal guidewires and catheter devices by using remotely controlled technology. Performing tele-R-PCI from a remote location via fifth generation network communication technology has never been reported in China; however, if this were possible, the technique could be used to treat many patients with coronary artery disease who would otherwise not have the opportunity of treatment. The case of a 73-year-old male patient with coronary artery disease who underwent successful tele-R-PCI at 800 km from the operators is presented. Performing long-distance tele-R-PCI in patients with coronary artery disease is feasible with predictably successful outcomes when reliable network connectivity and local cardiac catheterization facilities are present.

OBJECTIVE: To explore whether the differentiation of vascular stem cells (VSC) into smooth muscle cells (SMC) in aortic dissection (AD) is dysregulated, and to verify the role of Notch3 pathway in this process. METHODS: Aortic tissues were obtained from AD patients undergoing aortic vascular replacement and heart transplant donors at Department of Cardiovascular Surgery, Guangdong Provincial People's Hospital Affiliated to Southern Medical University. VSC were isolated by enzymatic digestion and c-kit immunomagnetic beads. The cells were divided into normal donor-derived VSC group (Ctrl-VSC group) and AD-derived VSC group (AD-VSC group). The presence of VSC in the aortic adventitia was detected by immunohistochemical staining, and VSC was identified by stem cell function identification kit. The differentiation model of VSC into SMC established in vitro was induced by transforming growth factor-β1 (10 μg/L) for 7 days. They were divided into normal donor VSC-SMC group (Ctrl-VSC-SMC group), AD VSC-SMC group (AD-VSC-SMC group) and AD VSC-SMC+Notch3 inhibitor DAPT group (AD-VSC-SMC+DAPT group,DAPT 20 μmol/L was added during differentiation induction). The expression of contractile marker Calponin 1 (CNN1) in SMC derived from aortic media and VSC were detected by immunofluorescence staining. The protein expressions of contractile markers α-smooth muscle actin (α-SMA), CNN1 as well as Notch3 intracellular domain (NICD3) in SMC derived from aortic media and VSC were detected by Western blotting. RESULTS: Immunohistochemical staining showed there was a population of c-kit-positive VSC in the adventitia of aortic vessels, and VSC from both normal donors and AD patients had the ability to differentiate into adipocytes and chondrocytes. Compared with normal donor vascular tissue, the expressions of SMC markers α-SMA and CNN1 of tunica media contraction in AD were down-regulated (α-SMA/β-actin: 0.40±0.12 vs. 1.00±0.11, CNN1/β-actin: 0.78±0.07 vs. 1.00±0.14, both P < 0.05), while the protein expression of NICD3 was up-regulated (NICD3/GAPDH: 2.22±0.57 vs. 1.00±0.15, P < 0.05). Compared with Ctrl-VSC-SMC group, the expressions of contractile SMC markers α-SMA and CNN1 were down-regulated in AD-VSC-SMC group (α-SMA/β-actin: 0.35±0.13 vs. 1.00±0.20, CNN1/β-actin: 0.78±0.06 vs. 1.00±0.07, both P < 0.05), the protein expression of NICD3 was up-regulated (NICD3/GAPDH: 22.32±1.22 vs. 1.00±0.06, P < 0.01). Compared with AD-VSC-SMC group, the expressions of contractile SMC markers α-SMA, CNN1 were up-regulated in AD-VSC-SMC+DAPT group (α-SMA/β-actin: 1.70±0.07 vs. 1.00±0.15, CNN1/β-actin: 1.62±0.03 vs. 1.00±0.02, both P < 0.05). CONCLUSIONS Dysregulation of VSC differentiation into SMC occurs in AD, while inhibition of Notch3 pathway activation can restore the expression of contractile proteins in VSC-derived SMC in AD.
Humans ; Actins ; Platelet Aggregation Inhibitors ; Signal Transduction ; Aortic Dissection ; Cell Differentiation ; Myocytes, Smooth Muscle ; Stem Cells